query: cells attracted to the site of infection by il-8 are

pos: Interleukin 8 down the ECM and basement membrane. These are released in secretory granules, along with more integrins. The release of ROS and damaging enzymes is regulated to minimise host damage, but continues to reach site of infection at which it will carry out its effector functions. While neutrophil granulocytes are the primary target cells of IL-8, there are a relatively wide range of cells (endothelial cells, macrophages, mast cells, and keratinocytes) that respond to this chemokine. The chemoattractant activity of IL-8 in similar concentrations to vertebrates was proven in Tetrahymena pyriformis, which suggests a phylogenetically well-conserved structure and function for this

pos: Leukocyte extravasation activation by pathogens, resident macrophages in the affected tissue release cytokines such as IL-1, TNFα and chemokines. IL-1, TNFα and C5a cause the endothelial cells of blood vessels near the site of infection to express cellular adhesion molecules, including selectins. Circulating leukocytes are localised towards the site of injury or infection due to the presence of chemokines. Like velcro, carbohydrate ligands on the circulating leukocytes bind to selectin molecules on the inner wall of the vessel, with marginal affinity. This causes the leukocytes to slow down and begin rolling along the inner surface of the vessel wall. During this rolling

pos: Interleukin 17 Reduced regulation allows uninhibited proliferation of Th17 cells and production of IL-17 in psoriatic lesions, augmenting IL-17 signaling. Antimicrobial peptides and IL-8 attract neutrophils to the site of injury where these cells remove damaged and inflamed keratinocyte cells. New immature DCs are also recruited by CCL20 via chemotaxis where their activation restarts and amplifies the cycle of inflammation. IL-17 and additional cytokines released from the influx of neutrophils, T and dendritic cells mediate effects on localized leukocytes and keratinocytes that supports the progression of psoriasis by inciting chronic inflammation. The IL-17F gene was discovered in 2001, and is located on

pos: Interferon type II IFN-γ. The presence of IFN-γ in T helper cells makes that undifferentiated CD4+ cells (Th0 cells) to differentiated into Th1 cells. Therefore, there is a positive feedback loop which suppress Th2 cell differentiation. The defense against an infection is led by NK cells when they secrete the interferon, whereas the adaptative immune response is directed by mainly T lymphocytes with interferon-gamma. APCs release a sort of cytokines that control the production of IFN-gamma. This cytokines are IL-12 and IL-18 which serve to connect the infection with IFN-gamma production in the innate immunity response. Once macrophages recognize pathogens, it causes the

pos: Natural killer cell to the NK cell the presence of viral pathogens in the affected area. Cytokines involved in NK activation include IL-12, IL-15, IL-18, IL-2, and CCL5. NK cells are activated in response to interferons or macrophage-derived cytokines. They serve to contain viral infections while the adaptive immune response generates antigen-specific cytotoxic T cells that can clear the infection. NK cells work to control viral infections by secreting IFNγ and TNFα. IFNγ activates macrophages for phagocytosis and lysis, and TNFα acts to promote direct NK tumor cell killing. Patients deficient in NK cells prove to be highly susceptible to early phases of

pos: Testicular immunology fine detail, the course of testicular events during a bacterial infection. In the short term (3 hours) multiple inflammatory factors are produced and released by testicular macrophages. Examples are prostaglandin E2, inducible nitric oxide synthase (iNOS), TNFα and IL-1β, although at lower levels than other tissues. Non-immune cells of the testis such as Sertoli cells and Leydig cells also able to respond to bacteria. During a bacterial infection, testosterone levels and the amount of testicular interstitial fluid are reduced. Neutrophils enter the testis about 12 hours after infection. Importantly, there is damage to the developing sperm, which start to die

pos: Interleukin 8 a potent promoter of angiogenesis. In target cells, IL-8 induces a series of physiological responses required for migration and phagocytosis, such as increases in intracellular Ca, exocytosis (e.g. histamine release), and the respiratory burst. IL-8 can be secreted by any cells with toll-like receptors that are involved in the innate immune response. Usually, it is the macrophages that see an antigen first, and thus are the first cells to release IL-8 to recruit other cells. Both monomer and homodimer forms of IL-8 have been reported to be potent inducers of the chemokine receptors CXCR1 and CXCR2. The homodimer is more

pos: TLR9 a hypoxic cellular environment. This environment causes the release of mitochondrial DNA, which has CpG regions that can bind to TLR9. This induces over-expression of TLR9 in tumor cells, contrary to the inhibitory early stages of infection. Epstein-Barr virus, like other oncogenic viruses, decreases the expression of TLR9 in B cells, diminishing production of TNF and IL-6. EBV has been reported to alter expression of TLR9 at the transcription, translation, and protein level. The viruses of the polyomavirus family destroy expression of TLR9 in keratinocytes, inhibiting the release of IL-6 and IL-8. Expression is regulated at the promoter, where antigen

pos: Interleukin-1 family which the mechanism and regulation are not known. IL-1 is intensely produced by tissue macrophages, monocytes, fibroblasts, and dendritic cells, but is also expressed by B lymphocytes, NK cells, microglia, and epithelial cells. They form an important part of the inflammatory response of the body against infection. These cytokines increase the expression of adhesion factors on endothelial cells to enable transmigration (also called diapedesis) of immunocompetent cells, such as phagocytes, lymphocytes and others, to sites of infection. They also affect the activity of the hypothalamus, the thermoregulatory center, which leads to a rise in body temperature (fever) . That is

pos: Interleukin 8 Interleukin 8 Interleukin 8 (IL8 or chemokine (C-X-C motif) ligand 8, CXCL8) is a chemokine produced by macrophages and other cell types such as epithelial cells, airway smooth muscle cells and endothelial cells. Endothelial cells store IL-8 in their storage vesicles, the Weibel-Palade bodies. In humans, the interleukin-8 protein is encoded by the "CXCL8" gene. IL-8 is initially produced as a precursor peptide of 99 amino acids which then undergoes cleavage to create several active IL-8 isoforms. In culture, a 72 amino acid peptide is the major form secreted by macrophages. There are many receptors on the surface membrane capable

pos: T helper 17 cell are IL-17A, IL-17F, IL-21, and IL-22, as well as granulocyte-macrophage colony-stimulating factor (GM-CSF). IL-17 family cytokines (IL-17A and IL-17F) target innate immune cells and epithelial cells, among others, to produce G-CSF and IL-8 (CXCL8), which leads to "neutrophil" production and recruitment. In this way, T17 cell lineage appears to be one of the three major subsets of effector T cells, as these cells are involved in regulation of neutrophils, while Th2 cells regulate eosinophils, basophils and mast cells, and Th1 cells regulate macrophages and monocytes. Thus, three T helper cell subsets are able to influence the myeloid part of the

pos: Interleukin 18 Interleukin 18 Interleukin-18 (IL18, also known as interferon-gamma inducing factor) is a protein which in humans is encoded by the "IL18" gene. The protein encoded by this gene is a proinflammatory cytokine. IL-18 is a cytokine that belongs to the IL-1 superfamily and is produced by macrophages and other cells. IL-18 works by binding to the interleukin-18 receptor, and together with IL-12 it induces cell-mediated immunity following infection with microbial products like lipopolysaccharide (LPS). After stimulation with IL-18, natural killer (NK) cells and certain T cells release another important cytokine called interferon-γ (IFN-γ) or type II interferon that plays an

pos: Interleukin-8 receptor threonine residues (a characteristic of many proteins of the 7-transmembrane G-protein coupled receptor family). The C-terminus is a target for phosphorylation and exhibits kinase activity. This is the beginning of signaling pathways and phosphorylation cascades to recruit neutrophils and angiogenesis, the development and growth of new blood vessels. Both IL-8RA and IL-8RB are expressed in neutrophils, monocytes, macrophages, basophils, T-lymphocytes, and endothelial cells. IL-8RB is expressed additionally in neurons of the central nervous system. IL-8RA is highly specific for interleukin-8 and only responds when this particular ligand is bound to its receptor site, exhibiting "specific" binding behavior. IL-8RB binds to

pos: Interleukin 13 Studies on transgenic mouse in vivo demonstrate that lung over-expression of IL-13 induces subepithelial airway fibrosis. IL-13 is the dominant effector in toxin, infection, allergic, and post-transplant bronchiolitis obliterans models of fibrosis. Other research suggests that IL-13 is responsible for the promotion of the survival and the migration of epithelial cells, production of inducible nitric oxide synthase by airway epithelial cells, activation of macrophages, permeability of the epithelial cells, production of inducible nitric oxide synthase by airway epithelial cells, and transformation of airway fibroblasts to myofibroblasts leading to collagen deposition. The deposition then influences the airway remodelling in asthmatic patients.

pos: Interleukin 17 entering the final stages of their cell cycle, which activates immature dendritic cells (DC). Cytokines released from DCs stimulate dying keratinocytes to secrete TNF-alpha, IL-1 and IL-6 leading to the chemotaxis of T cells, natural killer cells and monocytes to the epidermis. These cells release IL-23 which induce Th17 cells to produce IL-17. IL-17 interaction with IL-17RA receptors, abundant on the keratinocyte cell surface, incite epidermal cells to increase expression of IL-6, antimicrobial peptides, IL-8 and CCL20. Increased concentration of IL-6 alters the epidermal environment by decreasing the ability of T regulatory cells to control the behavior of Th17 cells.

pos: Phagocyte located in the tissue near the infection site. Another group of chemical attractants are cytokines that recruit neutrophils and monocytes from the blood. To reach the site of infection, phagocytes leave the bloodstream and enter the affected tissues. Signals from the infection cause the endothelial cells that line the blood vessels to make a protein called selectin, which neutrophils stick to on passing by. Other signals called vasodilators loosen the junctions connecting endothelial cells, allowing the phagocytes to pass through the wall. Chemotaxis is the process by which phagocytes follow the cytokine "scent" to the infected spot. Neutrophils travel across

pos: Pathogenic fungus Studies have shown that hosts with higher levels of immune response cells such as monocytes/macrophages, dendritic cells, and invariant natural killer (iNK) T-cells exhibited greater control of fungal growth and protection against systemic infection. Pattern recognition receptors (PRRs) play an important role in inducing an immune response by recognizing specific fungal pathogens and initiating an immune response. In the case of mucosal candidiasis, the cells that produce cytokine IL-17 are extremely important in maintaining innate immunity. Pathogenic fungus Pathogenic fungi are fungi that cause disease in humans or other organisms. Approximately 300 fungi are known to be pathogenic to humans.

pos: Cytokine up to 1,000 times during trauma or infection. The widespread distribution of cellular sources for cytokines may be a feature that differentiates them from hormones. Virtually all nucleated cells, but especially endo/epithelial cells and resident macrophages (many near the interface with the external environment) are potent producers of IL-1, IL-6, and TNF-α. In contrast, classic hormones, such as insulin, are secreted from discrete glands (e.g., the pancreas). The current terminology refers to cytokines as immunomodulating agents. A contributing factor to the difficulty of distinguishing cytokines from hormones is that some immunomodulating effects of cytokines are systemic rather than local. For

pos: Neutrophil inflammation. They migrate through the blood vessels, then through interstitial tissue, following chemical signals such as Interleukin-8 (IL-8), C5a, fMLP, Leukotriene B4 and HO in a process called chemotaxis. They are the predominant cells in pus, accounting for its whitish/yellowish appearance. Neutrophils are recruited to the site of injury within minutes following trauma and are the hallmark of acute inflammation; however, due to some pathogens being indigestible, they can be unable to resolve certain infections without the assistance of other types of immune cells. When adhered to a surface, neutrophil granulocytes have an average diameter of 12–15 micrometers (µm) in

pos: Interleukin 17 as IL-6, G-CSF, GM-CSF, IL-1β, TGF-β, TNF-α), chemokines (including IL-8, GRO-α, and MCP-1), and prostaglandins (e.g., PGE) from many cell types (fibroblasts, endothelial cells, epithelial cells, keratinocytes, and macrophages). IL-17 acts with IL-22 (produced by T helper 17 cells) to induce expression of antimicrobial peptide by keratinocytes. The release of cytokines causes many functions, such as airway remodeling, a characteristic of IL-17 responses. The increased expression of chemokines attracts other cells including neutrophils but not eosinophils. IL-17 function is also essential to a subset of CD4+ T-Cells called T helper 17 (T17) cells. As a result of these roles, the

pos: Allergic bronchopulmonary aspergillosis infection such as pleuritic chest pain and fever. Patients with asthma and symptoms of ongoing infection, who do not respond to antibiotic treatment, should be suspected of ABPA. "Aspergillus" spores are small (2–3 μm in diameter) and can penetrate deep into the respiratory system to the alveolar level. In healthy people, innate and adaptive immune responses are triggered by various immune cells (notably neutrophils, resident alveolar macrophages and dendritic cells) drawn to the site of infection by numerous inflammatory cytokines and neutrophilic attractants (such as CXCR2 receptor ligands). In this situation, mucociliary clearance is initiated and spores are successfully phagocytosed,

pos: Interleukin 23 subunit alpha Interleukin 23 subunit alpha Interleukin-23 subunit alpha is a protein that in humans is encoded by the "IL23A" gene. IL-23 is produced by dendritic cells and macrophages. Interleukin-23 is a heterodimeric cytokine composed of an IL-12p40 subunit that is shared with IL-12 and the IL-23p19 subunit. A functional receptor for IL-23 (the IL-23 receptor) has been identified and is composed of IL-12R β1 and IL-23R. IL-23 is an important part of the inflammatory response against infection. It promotes upregulation of the matrix metalloprotease MMP9, increases angiogenesis and reduces CD8+ T-cell infiltration into tumours. IL-23 mediates its effects on both innate

pos: Interleukin 27 transcription factors that bind specifically to the receptor subunits, IL-27ɑ and glycoprotein. IL-27 is able to activate STAT3 signaling, which eventually leads to an increase of IL-10 secretion from Treg cells. IL-27 plays a crucial role in mycobacterium tuberculosis infection. IL-27 inhibits IFN-gamma induced autophagy by activating PI3K/Akt/mTOR pathway and up-regulation of an anti apoptotic protein Mcl-1, in Mycobacterium tuberculosis H37Rv strain infected human macrophages. Interleukin 27 Interleukin 27 (IL-27) is a member of the IL-12 cytokine family. It is a heterodimeric cytokine that is composed of two distinct genes, Epstein-Barr virus-induced gene 3 (EBI3) and IL-27p28. IL-27 is expressed

pos: Interleukin 10 shown to induce IFNγ and CD8+ T cell dependent anti-tumor immunity. More specifically, PEGylated recombinant human IL-10 (PEG-rHuIL-10) has been shown to enhance CD8+ T cell secretion of the cytotoxic molecules Granzyme B and Perforin and potentiate T cell receptor dependent IFNγ secretion. A study in mice has shown that IL-10 is also produced by mast cells, counteracting the inflammatory effect that these cells have at the site of an allergic reaction. IL-10 is capable of inhibiting synthesis of pro-inflammatory cytokines such as IFN-γ, IL-2, IL-3, TNFα and GM-CSF made by cells such as macrophages and Th1 T cells. It

pos: Cladophialophora carrionii the fungus by growing it on an agar plate and observing the colony morphology and sporulation characteristics. However, "C. carrionii" grows quite slowly in culture, so significant results cannot be obtained until after 4–6 weeks of incubation. During infection, the immune system of the host attempts to eliminate the fungus via engulfment and degradation by macrophages and neutrophils, which function in the innate immune system. The adaptive immune system also plays a role by activating cells such as interleukin-6 (IL-6), the type of IL specifically produced with "C. carrionii" infection, but it may have negative consequences for eradicating the fungus.

pos: Bone healing or immobilisation, external fixation, or internal fixation. There are three major phases of fracture healing, two of which can be further sub-divided to make a total of five phases: After bone fracture, blood cells accumulate adjacent to the injury site. Soon after fracture, blood vessels constrict, stopping further bleeding. Within a few hours, the extravascular blood cells form a clot called a hematoma that acts as a template for callus formation. These cells, including macrophages, release inflammatory mediators such as cytokines (tumor necrosis factor alpha (TNFα), interleukin-1 family (IL-1), interleukin 6 (IL-6), 11 (IL-11), and 18 (IL-18)) and increase blood

pos: Granulocyte release another substance called prostaglandins that contributes to an increased blood flow to the site of infection. Both of these mechanisms allow blood-clotting elements to be delivered to the infected area (this begins the recovery process and blocks the travel of microbes to other parts of the body). Increased permeability of the inflamed tissue also allows for more phagocyte migration to the site of infection so that they can consume microbes. Mast cells are a type of granulocyte that are present in tissues; they mediate host defense against pathogens (e.g., parasites) and allergic reactions, particularly anaphylaxis. Mast cells are also

pos: Leishmania and corrupt it for their own benefit. They use the willingly phagocytosing polymorphonuclear neutrophil granulocytes (PMNs) rigorously as a tricky hideout, where they proliferate unrecognized from the immune system and enter the long-lived macrophages to establish a "hidden" infection. Upon microbial infection, PMNs move out from the bloodstream through the vessels’ endothelial layer, to the site of the infected tissue (dermal tissue after fly bite). They immediately initiate the first immune response and phagocytize the invader by recognition of foreign and activating surfaces on the parasite. Activated PMN secrete chemokines, IL-8 particularly, to attract further granulocytes and stimulate phagocytosis. Further,

pos: Melanocyte MHC, but most cells only express MHC class I. The other class of MHC, Class II, is found only on "professional" antigen presenting cells such as dendritic cells, macrophages, B cells, and melanocytes. Importantly, melanocytes stimulated by cytokines express surface proteins such as CD40 and ICAM1 in addition to MHC class II, allowing for co-stimulation of T cells. In addition to presenting antigen, one of the roles of melanocytes in the immune response is cytokine production. Melanocytes express many proinflammatory cytokines including IL-1, IL-3, IL-6, IL-8, TNF-α, and TGF-β. Like other immune cells, melanocytes secrete these cytokines in response to

pos: Allergic conjunctivitis inflammatory cells. When histamine is released from mast cells, it binds to H1 receptors on nerve endings and causes the ocular symptom of itching. Histamine also binds to H1 and H2 receptors of the conjunctival vasculature and causes vasodilatation. Mast cell-derived cytokines such as chemokine interleukin IL-8 are involved in recruitment of neutrophils. TH2 cytokines such as IL-5 recruit eosinophils and IL-4, IL-6, and IL-13, which promote increased sensitivity. Immediate symptoms are due to the molecular cascade. Encountering the allergen a patient is sensitive to leads to increased sensitization of the system and more powerful reactions. Advanced cases can progress

neg: Inflammation include prostaglandins, inflammatory cytokines such as IL-1β, TNF-α, IL-6 and IL-15 and chemokines such as IL-8 and GRO-alpha. These inflammatory mediators, and others, orchestrate an environment that fosters proliferation and survival. Inflammation also causes DNA damages due to the induction of reactive oxygen species (ROS) by various intracellular inflammatory mediators. In addition, leukocytes and other phagocytic cells attracted to the site of inflammation induce DNA damages in proliferating cells through their generation of ROS and reactive nitrogen species (RNS). ROS and RNS are normally produced by these cells to fight infection. ROS, alone, cause more than 20 types of DNA

neg: Microglia the extracellular space. This activates more microglia and starts a cytokine induced activation cascade rapidly activating all nearby microglia. Microglia-produced TNF-α causes neural tissue to undergo apoptosis and increases inflammation. IL-8 promotes B-cell growth and differentiation, allowing it to assist microglia in fighting infection. Another cytokine, IL-1, inhibits the cytokines IL-10 and TGF-β, which downregulate antigen presentation and pro-inflammatory signaling. Additional dendritic cells and T-cells are recruited to the site of injury through the microglial production of the chemotactic molecules like MDC, IL-8, and MIP-3β. Finally, PGE and other prostanoids prevent chronic inflammation by inhibiting microglial pro-inflammatory response and downregulating

neg: Interleukin 8 of binding IL-8; the most frequently studied types are the G protein-coupled serpentine receptors CXCR1 and CXCR2. Expression and affinity for IL-8 differs between the two receptors (CXCR1 > CXCR2). Through a chain of biochemical reactions, IL-8 is secreted and is an important mediator of the immune reaction in the innate immune system response. IL-8, also known as "neutrophil chemotactic factor", has two primary functions. It induces chemotaxis in target cells, primarily neutrophils but also other granulocytes, causing them to migrate toward the site of infection. IL-8 also stimulates phagocytosis once they have arrived. IL-8 is also known to be

neg: Cholinergic anti-inflammatory pathway anti-inflammatory pathway as well. Tumor necrosis factors (TNF) (and other cytokines) are produced by cells of the innate immune system during local injury and infection. These contribute to initiating a cascade of mediator release, and recruiting inflammatory cells to the site of infection to contain infection, referred to as "innate immunity.". TNF amplifies and prolongs the inflammatory response by activating other cells to release interleukin-1 (IL-1), high mobility group B1 (HMGB1) and other cytokines. These inflammatory cytokine responses confer protective advantages to the host at the site of bacterial infection. A “beneficial” inflammatory response is limited, resolves in 48–72 hours,

neg: HHV-8-associated MCD HHV-8 are seen most frequently in the setting of immune dysfunction related to factors such as HIV infection or use of immunosuppressant medications; however, HHV-8-associated diseases, including HHV-8-associated MCD, have been reported in otherwise healthy individuals. In HHV-8-associated MCD the HHV-8 virus infects B cells and plasmablasts in lymph nodes and causes infected cells to release proinflammatory cytokines, signaling molecules that increase the activity of immune cells. In particular, HHV-8 infection of immune cells leads to increased levels of Interleukin-6 (IL-6), a cytokine known to play a role in other forms of Castleman disease. The HHV-8 virus contains a gene

neg: Interleukin 4 IL-4 may also play a role in the infection and development of HIV disease. Auxiliary T-lymphocytes are a key element of HIV-1 infection. Several signs of immune dysregulation such as polyclonal B-cell initialization, previous cell-mediated antigen-induced response and hypergammaglobulinaemia occur in most HIV-1 infected patients and are associated with cytokines synthesized by Th2 cells. Increased IL-4 production by Th2 cells has been demonstrated in people infected with HIV. Interleukin 4 The interleukin 4 (IL4, IL-4) is a cytokine that induces differentiation of naive helper T cells (Th0 cells) to Th2 cells. Upon activation by IL-4, Th2 cells subsequently produce additional

neg: Th 9 cell HCV clearance was associated with lower T9 cytokines' leves. This might be caused by T9 mediated promotion of T17 phenotype and hindering of T1 phenotype which leads to persisting viral infection. There were several publications trying to elucidate role of T9 cells in chronic HBV infection with inconsistent results. Th 9 cell In cell biology, T9 cells (T helper type 9 cells, CD4+IL-9+IL-13−IFNγ − ) are a sub-population of CD4+T cells that produce interleukin-9 (IL-9). They play a role in defense against helminth infections, in allergic responses, in autoimmunity, and tumor suppression. T9 cells are characterized by their cell surface

neg: Plasmacytoid dendritic cell under study. Upon stimulation and subsequent activation of TLR7 and TLR9, these cells produce large amounts (up to 1,000 times more than other cell type) of type I interferon (mainly IFN-α and IFN-β), which are critical anti-viral compounds mediating a wide range of effects and induce maturation of the pDC. For example, the secretion of type 1 interferon triggers natural killer cells to produce IFNγ while also activating the differentiation of B cells. In addition, they can produce cytokines IL-12, IL-6 and TNF-α as well, helping to recruit other immune cells to the site of infection. Because they are capable

neg: Interleukin-8 receptor 8 release and to produce enzymes that would assist in the destruction of foreign material at the site of infection IL-8 receptors are 7-transmembrane proteins; they contain 7 alpha helices that each span the thickness of the phospholipid bilayer of a cell membrane. IL-8RA is a peptide of 350 amino acids, and IL-8RB is composed of 355 amino acids. Receptors A and B share 78% of their sequence identity, and are considered to be the only two biologically significant receptors of IL-8. The genes for both receptors are located on chromosome 2q35 and are each encoded by a single exon,

neg: Alveolar macrophage upon activation by bacterial products. Apoptosis is particularly regulated by the presence of cytokines: IFN-γ increases the rate of apoptosis, whereas IL-10 and TGF-β decrease it. However, IL-10 has counterproductive effects on the immune system, and has been shown to actually promote infection by foreign pathogens. The role of IL-10 in bacterial and parasitic infection has been discovered as a strategy to evade host immune systems. There are bacteria which parasitize AMs by invading through their membranes, and thrive by growing and replicating inside of them, exploiting AMs as host cells. Normally, this infection can be eliminated by T-cells, which

neg: Pulpitis levels of interleukin 8 (IL-8) and genes related to chemokines and chemokine receptors. The odontoblasts have been shown to attract immature dendritic cells. Dendritic cells (DCs) are a heterogeneous leukocyte (white blood cell) population. DCs in healthy peripheral tissues (steady state) are in an immature state. The cells are capable of sensing microbes as well as antigen capture and processing capabilities. A rapid accumulation of pulpal DCs has been observed beneath cavity preparations, and an increased number of DCs accumulated under caries. Immature DCs are therefore considered to be part of the innate phase of pulpal immune response. Persistent infection

neg: Interleukin 8 potent, but methylation of Leu25 can block the activity of homodimers. IL-8 is believed to play a role in the pathogenesis of bronchiolitis, a common respiratory tract disease caused by viral infection. IL-8 is a member of the CXC chemokine family. The genes encoding this and the other ten members of the CXC chemokine family form a cluster in a region mapped to chromosome 4q. CXCL8 is the primary cytokine involved in the recruitment of neutrophils to the site of damage or infection; in a process called chemotaxis. A number of variables are essential for the successful chemotaxis of neutrophils,

neg: IL17A in viral infection such as influenza through promoting neutrophilic inflammation. The requirements of IL-17A and IL-17 receptor signaling in host defense were well documented and appreciated before the identification of Th17 cells as an independent T helper cell lineage. In experimental pneumonia models, IL-17A or IL-17RA knock mice have increased susceptibility to various Gram-negative bacteria, such as Klebsiella pneumoniae and Mycoplasma pneumonia. In contrast, data suggest that IL-23 and IL-17A are not required for protection against primary infection by the intracellular bacteria Mycobacterium tuberculosis. Both the IL-17RA knock out mice and the IL-23p19 knock out mice cleared primary infection with

neg: ILC2 helper 2 cells. ILC2s play the crucial role of secreting type 2 cytokines in response to helminth infection. They have also been implicated in the development of allergic lung inflammation. They express characteristic surface markers and receptors for chemokines, which are involved in distribution of lymphoid cells to specific organ sites. They require IL-7 for their development, which activates two transcription factors (both required by these cells)—RORα and GATA3. After stimulation with Th2 polarising cytokines (e.g. IL-25, IL-33, TSLP) ILC2s start to produce IL-5, IL-13, IL-9, IL-4. ILC2s are critical for primary responses to local Th2 antigens e.g. helmints and

neg: Chronic mucocutaneous candidiasis with the first CANDF1 being located at 2p22.3-p21(cytogenetically) The mechanism of the human immune system has it normally fighting in an infection (like "Candida"). Initially Th17 cells are made by the immune system, which in turn produces interleukin-17 (IL-17). Inflammation is induced and white blood cells confront infection. Chronic mucocutaneous candidiasis mutations affect IL-17 by inhibiting its pathway. This in turn affects the human immune systems ability to fight infection, in total there are 9 possible types of this condition. Chronic mucocutaneous candidiasis can be diagnosed in an affected individual via the following methods/tests: Management for an individual with chronic

neg: Innate lymphoid cell cytokines in response to helminth infection. They have also been implicated in the development of allergic lung inflammation. They express characteristic surface markers and receptors for chemokines, which are involved in distribution of lymphoid cells to specific organ sites. They require IL-7 for their development, which activates two transcription factors (both required by these cells)—RORα and GATA3. After stimulation with Th2 polarising cytokines (e.g. IL-25, IL-33, TSLP) ILC2s start to produce IL-5, IL-13, IL-9, IL-4. ILC2s are critical for primary responses to local Th2 antigens e.g. helminths and viruses and that is why ILC2s are abundant in tissues of skin,

neg: Tissue-resident memory T cell is dependent on the cytokine TGFβ. CD8+ effector T cells that lack TGFβ fail to upregulate CD103, and subsequently do not differentiate into TRM cells. The important role in development of TRM cells have various cytokines that support TRM cell formation and survival. For example homeostatic cytokine IL-15, pro-inﬂammatory cytokines such as IL-12 and IL-18, and barrier cytokines such as IL-33. TRM cells reside in many tissues that create barriers against outside environment and thus provide defense against incoming pathogens. In the skin, lung, brain, and vagina TRM cells are required to provide rapid control of infection and are more

neg: Bacterial effector protein secretion of interleukin-8 (IL-8), and thus affect the immune system (immunomodulation). EspG functions as a Rab GTPase-activating protein (Rab-GAP), trapping Rab-GTPases in their inactive GDP bound form, and reducing ER–Golgi transport (of IL-8 and other proteins). Apoptosis (programmed cell death). Apoptosis is usually a mechanism of defense to infection, given that apoptotic cells eventually attract immune cells to remove them and the pathogen. Many pathogenic bacteria have developed mechanisms to prevent apoptosis, not the least to maintain their host environment. For instance, the EPEC/EHEC effectors NleH and NleF block apoptosis. Similarly, the "Shigella" effectors IpgD and OspG (a homolog of

neg: Interleukin 21 where it was administered alone or coupled with drugs as sorafinib and rituximab. IL-21 may be a critical factor in the control of persistent viral infections. IL-21 (or IL-21R) knock-out mice infected with chronic LCMV (lymphocytic choriomeningitis virus) were not able to overcome chronic infection compared to normal mice. Besides, these mice with impaired IL-21 signaling had more dramatic exhaustion of LCMV-specific CD8+ T cells, suggesting that IL-21 produced by CD4+ T cells is required for sustained CD8+ T cell effector activity and then, for maintaining immunity to resolve persistent viral infection. Thus, IL-21 may contribute to the mechanism by

neg: Superantigen of antigen presenting cells and T-cells elicits a response that is mainly inflammatory, focused on the action of Th1 T-helper cells. Some of the major products are IL-1, IL-2, IL-6, TNF-α, gamma interferon (IFN-γ), macrophage inflammatory protein 1α (MIP-1α), MIP-1β, and monocyte chemoattractant protein 1 (MCP-1). This excessive uncoordinated release of cytokines, (especially TNF-α), overloads the body and results in rashes, fever, and can lead to multi-organ failure, coma and death. Deletion or anergy of activated T-cells follows infection. This results from production of IL-4 and IL-10 from prolonged exposure to the toxin. The IL-4 and IL-10 downregulate production of

neg: Tuft cell Tuft cell Tuft cells, sometimes referred to as brush cells, are chemosensory cells in the epithelial lining of the intestines and respiratory tract. The names "tuft" and "brush" refer to the microvilli projecting from the cells. Ordinarily there are very few tuft cells present but they have been shown to greatly increase at times of a parasitic infection. Several studies have proposed a role for tuft cells in defense against parasitic infection. In the intestine, tuft cells are the sole source of secreted interleukin 25 (IL-25). Tuft cells are differentiated from stem cells in the bases of intestinal glands and

neg: Tuft cell in the mouse stomach. Tuft cell Tuft cells, sometimes referred to as brush cells, are chemosensory cells in the epithelial lining of the intestines and respiratory tract. The names "tuft" and "brush" refer to the microvilli projecting from the cells. Ordinarily there are very few tuft cells present but they have been shown to greatly increase at times of a parasitic infection. Several studies have proposed a role for tuft cells in defense against parasitic infection. In the intestine, tuft cells are the sole source of secreted interleukin 25 (IL-25). Tuft cells are differentiated from stem cells in the bases

neg: Interleukin 15 Interleukin 15 Interleukin-15 (IL-15) is a cytokine with structural similarity to Interleukin-2 (IL-2). Like IL-2, IL-15 binds to and signals through a complex composed of IL-2/IL-15 receptor beta chain (CD122) and the common gamma chain (gamma-C, CD132). IL-15 is secreted by mononuclear phagocytes (and some other cells) following infection by virus(es). This cytokine induces cell proliferation of natural killer cells; cells of the innate immune system whose principal role is to kill virally infected cells. IL-15 was discovered in 1994 by two different laboratories, and characterized as T cell growth factor. Together with Interleukin-2 (IL-2), Interleukin-4 (IL-4), Interleukin-7 (IL-7), Interleukin-9

neg: ILC2 ILC2 ILC2 cells, or type 2 innate lymphoid cells are a type of innate lymphoid cell. They are derived from common lymphoid progenitor and belong to the lymphoid lineage. These cells lack antigen specific B or T cell receptor because of the lack of recombination activating gene. ILC2s produce type 2 cytokines (e.g. IL-4, IL-5, IL-9, IL-13). The cell type were first described in 2001. In 2006, a similar cell population was identified in a case of helminthic infection. The name "ILC2" was not proposed until 2013. They were previously identified in literature as natural helper cells, nuocytes, or innate

neg: Interleukin 15 track status by the FDA in 2017 and at that time, Phase III trials in bladder cancer were being prepared. Interleukin 15 Interleukin-15 (IL-15) is a cytokine with structural similarity to Interleukin-2 (IL-2). Like IL-2, IL-15 binds to and signals through a complex composed of IL-2/IL-15 receptor beta chain (CD122) and the common gamma chain (gamma-C, CD132). IL-15 is secreted by mononuclear phagocytes (and some other cells) following infection by virus(es). This cytokine induces cell proliferation of natural killer cells; cells of the innate immune system whose principal role is to kill virally infected cells. IL-15 was discovered in 1994

neg: Interleukin 13 however, the eventual result is organ damage and often profound or even fatal disease, not resolution of the infection. An emerging concept is that IL-13 may antagonize Th1 responses that are required to resolve intracellular infections. In this immune dysregulated context, marked by the recruitment of aberrantly large numbers of Th2 cells, IL-13 inhibits the ability of host immune cells to destroy intracellular pathogens. IL-13 expression has demonstrated to be increased in bronchoalveolar lavage (BAL) fluid and cells in patients with atopic mild asthma after allergen challenge. Genome-wide association studies have identified multiple polymorphisms of IL-13 and genes encoding the

neg: T helper 17 cell HIV infection (Gosselin et al. J Immunol 2010). The active form of vitamin D (1,25-Dihydroxyvitamin D3) has been found to 'severely impair' production of the IL-17 and IL-17F cytokines by Th17 cells. Thus, active form of vitamin D is a direct inhibitor for Th17 differentiation. In this way, oral administration of vitamin D3 was proposed to be a promising tool for the treatment of Th17-mediated diseases. In young patients with asthma 1,25-Dihydroxyvitamin D3-treated dendritic cells significantly reduced the percentage of Th17 cells, as well as IL-17 production. T helper 17 cell T helper 17 cells (T17) are a subset of

neg: Interleukin-8 receptor Interleukin-8 receptor The interleukin-8 receptors (IL-8R) are two 7-transmembrane proteins in the G-protein coupled-receptor family: interleukin-8 receptor A (IL-8RA) and interleukin-8 receptor B (IL-8RB). These receptors are generally found on human neutrophils, a type of white blood cell of the myeloid lineage, with approximately 65,000 receptors per neutrophil. Both receptors have a size of 60kDa, are glycosylated (contains covalent attachments and modifications) and G-protein linked, and can cause an increase in intracellular Ca levels. Binding of Interleukin 8 leads to activation of the cell (commonly a neutrophil), allowing it to recruit more white blood cells to the site of Interleukin

neg: Mucosal associated invariant T cell IL-12, IL-18, and IL-23, MAIT cells can produce and secrete pro-inflammatory cytokines, drawing immune cells into areas of the autoimmune attack. In this way, MAIT cells facilitate and intensify the harmful effects of systematic autoimmune rheumatic diseases. Mucosal associated invariant T cell Mucosal associated invariant T cells (MAIT cells) make up a subset of T cells in the immune system that display innate, effector-like qualities. In humans, MAIT cells are found in the blood, liver, lungs, and mucosa, defending against microbial activity and infection. The MHC class I-like protein, MR1, is responsible for presenting bacterially-produced vitamin B metabolites to MAIT

neg: Memory T cell Like naive T cells, T cells are CD45RO−, CCR7+, CD45RA+, CD62L+ (L-selectin), CD27+, CD28+ and IL-7Rα+, but they also express large amounts of CD95, IL-2Rβ, CXCR3, and LFA-1, and show numerous functional attributes distinctive of memory cells. Antigen-specific memory T cells against viruses or other microbial molecules can be found in both T and T subsets. Although most information is currently based on observations in the cytotoxic T cells (CD8-positive) subset, similar populations appear to exist for both the helper T cells (CD4-positive) and the cytotoxic T cells. Memory T cell Memory T cells are a subset of infection- and

neg: Cortisol (IFN)-gamma, IFN-alpha, and tumor-necrosis-factor (TNF)-alpha by antigen-presenting cells (APCs) and T helper (Th)1 cells, but upregulates IL-4, IL-10, and IL-13 by Th2 cells. This results in a shift toward a Th2 immune response rather than general immunosuppression. The activation of the stress system (and resulting increase in cortisol and Th2 shift) seen during an infection is believed to be a protective mechanism which prevents an over-activation of the inflammatory response. Cortisol can weaken the activity of the immune system. It prevents proliferation of T-cells by rendering the interleukin-2 producer T-cells unresponsive to interleukin-1 (IL-1), and unable to produce the T-cell

neg: Interleukin 2 Interleukin 2 Interleukin-2 (IL-2) is an interleukin, a type of cytokine signaling molecule in the immune system. It is a 15,5 - 16 kDa protein that regulates the activities of white blood cells (leukocytes, often lymphocytes) that are responsible for immunity. IL-2 is part of the body's natural response to microbial infection, and in discriminating between foreign ("non-self") and "self". IL-2 mediates its effects by binding to IL-2 receptors, which are expressed by lymphocytes. IL-2 is a member of a cytokine family, each member of which has a four alpha helix bundle; the family also includes IL-4, IL-7, IL-9, IL-15

neg: Haptotaxis movement of the dendritic cells up a fixed chemical gradient. Other leukocytes also exhibit haptotactic movement: neutrophils undergo IL-8 mediated migration, while monocytes, basophils, eosinophils and some T cells are influenced by RANTES chemokines. In the autoimmune disorder rheumatoid arthritis and in osteoarthritis, the associated swelling and migration of neutrophils to the affected site has been shown to be linked to membrane bound midkine cytokine. This cytokine operates in a haptotactic fashion, attracting local neutrophils to the site of expression. Haptotaxis plays a role in organizing cells to form tissues and specific regions of those tissues. Fibronectin and laminin both

neg: Interleukin 12 NK cells. A child with Bacillus Calmette–Guérin and "Salmonella enteritidis" infection was found to have a large homozygous deletion within the IL-12 p40 subunit gene, precluding expression of functional IL-12 p70 cytokine by activated dendritic cells and phagocytes. As a result, IFNγ production by the child's lymphocytes was markedly impaired. This suggested that IL-12 is essential for protective immunity to intracellular bacteria such as mycobacteria and Salmonella. Support is lent to this idea by the observation that a receptor for IL-12 is important for IFNγ production by lymphocytes. T and NK cells from seven unrelated patients who had severe idiopathic

neg: XCR1 mice that lack Aire, demonstrating it as a important regulator of XCL1 production. Naive CD8+ T cells are prepared when tumors form by cross-presentation via XCR1+ DCs and as a result will require a lower threshold to respond to antigen. Memory CD8+ T lymphocytes (mCTLs) are activated first after infection and then are signaled by CXCR3, IL-12, and CXCL9 by other XCR1+ DCs. In order to make a powerful secondary infection response, cytokine and chemokine signaling between XCR1+ DCs and NK cells must occur. XCR1 The "C" sub-family of chemokine receptors contains only one member: XCR1, the receptor for XCL1

neg: Morphine immune system, display opiate receptors. Dendritic cells are responsible for producing cytokines, which are the tools for communication in the immune system. This same study showed that dendritic cells chronically treated with morphine during their differentiation produce more interleukin-12 (IL-12), a cytokine responsible for promoting the proliferation, growth, and differentiation of T-cells (another cell of the adaptive immune system) and less interleukin-10 (IL-10), a cytokine responsible for promoting a B-cell immune response (B cells produce antibodies to fight off infection). This regulation of cytokines appear to occur via the p38 MAPKs (mitogen-activated protein kinase)-dependent pathway. Usually, the p38 within the

neg: Human herpesvirus 6 on its host. It has been demonstrated that HHV-6 fosters the progression of HIV-1 upon coinfection in T cells. HHV-6 upregulates the expression of the primary HIV receptor CD4, thus expanding the range of HIV susceptible cells. Several studies also have shown that HHV-6 infection increases production of inflammatory cytokines that enhance in vitro expression of HIV-1, such as TNF-alpha, IL-1 beta, and IL-8. A more recent in vivo study shows HHV-6A coinfection to dramatically accelerate the progression from HIV to AIDS in pigtailed macaques. HHV-6 has also been demonstrated to transactivate Epstein–Barr virus. Humans acquire the virus at an

neg: Gluten immunochemistry intact. The release of IL15 is a major factor in coeliac disease as IL15 has been found to attract intraepithelial lymphocytes (IEL) that characterize Marsh grade 1 and 2 coeliac disease. Lymphocytes attracted by IL-15 are composed of markers enriched on natural killer cells versus normal helper T-cells. One hypothesis is that IL-15 induces the highly inflammatory Th1 response that activates T-helper cells (DQ2 restricted gliadin specific) that then orchestrate the destructive response, but the reason why inflammatory cells develop prior to gliadin specific helper cells is not known. The IRP response differs from typical responses that stimulate IL15 release,

neg: Neutrophil extracellular traps Neutrophil extracellular traps Neutrophil extracellular traps (NETs) are networks of extracellular fibers, primarily composed of DNA from neutrophils, which bind pathogens. Neutrophils are the immune system's first-line of defense against infection and have conventionally been thought to kill invading pathogens through two strategies: engulfment of microbes and secretion of anti-microbials. In 2004, a novel third function was identified: formation of NETs. NETs allow neutrophils to kill extracellular pathogens while minimizing damage to the host cells. Upon "in vitro" activation with the pharmacological agent phorbol myristate acetate (PMA), Interleukin 8 (IL-8) or lipopolysaccharide (LPS), neutrophils release granule proteins and chromatin to

neg: Neutrophil extracellular traps composed of host NET DNA. Neutrophil extracellular traps Neutrophil extracellular traps (NETs) are networks of extracellular fibers, primarily composed of DNA from neutrophils, which bind pathogens. Neutrophils are the immune system's first-line of defense against infection and have conventionally been thought to kill invading pathogens through two strategies: engulfment of microbes and secretion of anti-microbials. In 2004, a novel third function was identified: formation of NETs. NETs allow neutrophils to kill extracellular pathogens while minimizing damage to the host cells. Upon "in vitro" activation with the pharmacological agent phorbol myristate acetate (PMA), Interleukin 8 (IL-8) or lipopolysaccharide (LPS), neutrophils release

neg: GSDMD molecule for the lytic and highly inflammatory form of programmed cell death known as pyroptosis. Hence, GSDMD is an essential mediator of host defence against microbial infection and danger signals. The pore-forming activity of the N-terminal cleavage product causes cell swelling and lysis to prevent intracellular pathogens from replicating, and is required for the release of cytoplasmic content such as the inflammatory cytokine interleukin-1β (IL-1β) into the extracellular space to recruit and activate immune cells to the site of infection. GSDMD has an additional potential role as an antimicrobial by binding to cardiolipin (CL) and form pores on bacterial membranes.

neg: Asthma-related microbes (TNF)-α, interleukin (IL)-1β, IL-6 and IFN-γ by infected cells, which ultimately leads to immunopathological tissue damage and scarring in the asthmatic lungs. Furthermore, infection with "C. pneumonia" also induces serum immunoglobulin M (IgM), IgA, and IgG responses, which are associated with chronic asthma. "M. pneumoniae" is a bacterium that belongs to the phylum Firmicutes, class Mollicutes, order Mycoplasmatales and family Mycoplasmataceae. It is either filamentous or spherical. Individual spindle-shaped cells of "M. pneumoniae" are 1 to 2 µm long and 0.1 to 0.2 µm wide. "M. pneumoniae" is a motile, mesophilic bacterium that exhibits obligate aerobic respiration. It is an

neg: Soybean rust days. Weather conditions will determine when and where the spores travel from south to north. Rust spores, called Urediniospores, are able to penetrate the plant cells directly, rather than through natural openings or through wounds in the leaf tissue. Thus infection is relatively quick: about 9 to 10 days from initial infection to the next cycle of spore production. Rust is a multi-cyclic disease. After the initial infection is established, the infection site can produce spores for 10 to 14 days. Abundant spore production occurs during wet leaf periods (in the form of rain or dew) of at least 8

neg: Monocyte delay, of anti-inflammatory cytokines. Typical cytokines produced by monocytes are TNF, IL-1, and IL-12. A "monocyte count" is part of a complete blood count and is expressed either as a percentage of monocytes among all white blood cells or as absolute numbers. Both may be useful but these cells became valid diagnostic tools only when monocyte subsets are determined. Monocytosis is the state of excess monocytes in the peripheral blood. It may be indicative of various disease states. Examples of processes that can increase a monocyte count include: A high count of CD14+CD16++ monocytes is found in severe infection (sepsis)

neg: Leishmania "L. major" increases the secretion of IL-8 by PMNs. This mechanism is observed during infection with other obligate intracellular parasites, as well. For microbes like these, multiple intracellular survival mechanisms exist. Surprisingly, the coinjection of apoptotic and viable pathogens causes by far a more fulminate course of disease than injection of only viable parasites. When the anti-inflammatory signal phosphatidylserine usually found on apoptotic cells, is exposed on the surface of dead parasites, "L. major" switches off the oxidative burst, thereby preventing killing and degradation of the viable pathogen. In the case of "Leishmania", progeny are not generated in PMNs, but

neg: JAK-STAT signaling pathway can result in cancer and diseases affecting the immune system, such as severe combined immunodeficiency disorder (SCID). JAK3 can be used for the signalling of IL-2, IL-4, IL-15 and IL-21 (as well as other cytokines); therefore patients with mutations in the JAK3 gene often experience issues affecting many aspects of the immune system. For example, non-functional JAK3 causes SCID, which results in patients having no NK cells, B cells or T cells, and this would make SCID individuals susceptible to infection. Mutations of the STAT5 protein, which can signal with JAK3, has been shown to result in autoimmune disorders. It

neg: Resistin to) interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-12 (IL-12), and tumor necrosis factor-α (TNF-α) in an NF-κB-mediated (nuclear factor kappa-light-chain-enhancer of activated B cells-mediated) fashion. It has also been demonstrated that resistin upregulates intercellular adhesion molecule-1 (ICAM1) vascular cell-adhesion molecule-1 (VCAM1) and chemokine (C-C motif) ligand 2 (CCL2), all of which are occupied in chemotactic pathways involved in leukocyte recruitment to sites of infection. Resistin itself can be upregulated by interleukins and also by microbial antigens such as lipopolysaccharide, which are recognized by leukocytes. Taken together, because resistin is reputed to contribute to insulin resistance, results such as those mentioned suggest that

neg: T helper cell are the only cell group that expresses MHC Class II constitutively (at all times). Some APCs also bind native (or unprocessed) antigens to their surface, such as follicular dendritic cells, but unprocessed antigens do not interact with T cells and are not involved in their activation. The antigens that bind to MHC proteins are always short peptides, 8-10 amino acids long for MHC Class I, and up to 25 or so for MHC Class II. During an immune response, professional antigen-presenting cells (APCs) endocytose foreign material (typically bacteria or viruses), which undergoes processing, then travel from the infection site to

neg: Actinorhizal plant then between cortical cells. Later on "Frankia" becomes intracellular but no prenodule is formed. In both cases the infection leads to cell divisions in the pericycle and the formation of a new organ consisting of several lobes anatomically similar to a lateral root. This organ is the actinorhizal nodule also called actinorhizae. Cortical cells of the nodule are invaded by "Frankia" filaments coming from the site of infection or the prenodule. Actinorhizal nodules have generally an indeterminate growth, new cells are therefore continually produced at the apex and successively become infected. Mature cells of the nodule are filled with bacterial

neg: IL17A protection. Antigen specific CD4 T cells also limit nasopharyngeal colonization of S. pneumoniae in mouse models. Furthermore, immunization with pneumococcal whole cell antigen and several derivatives provided IL-17-mediated, but not antibody dependent, protection against S. pneumoniae challenge. In fungal infection, it has been shown an IL-17 producing clone with a TCR specific for calnexin from Blastomyces dermatitidis confers protection with evolutionary related fungal species including Histoplasma spp. In tumorigenesis, IL-17A has been shown to recruit myeloid derived suppressor cells (MDSCs) to dampen anti-tumor immunity. IL-17A can also enhance tumor growth in vivo through the induction of IL-6, which in turn

neg: Interleukin 7 in B and T cells, and increased recovery of T cells after cyclophosphamide administration or after bone marrow transplantation. IL-7 promotes hematological malignancies (acute lymphoblastic leukemia, T cell lymphoma). Elevated levels of IL-7 have also been detected in the plasma of HIV-infected patients. IL-7 as an immunotherapy agent has been examined in many pre-clinical animal studies and more recently in human clinical trials for various malignancies and during HIV infection. Recombinant IL-7 has been safely administered to patients in several phase I and II clinical trials. A human study of IL-7 in patients with cancer demonstrated that administration of this

neg: TLR4 been linked to accumulation and function of MDSC at the site of tumor and it also allows mesenchymal stromal cells to counter NK cell-mediated anti-tumor immunity. In HepG2 hepatoblastoma cells LPS increased TLR4 levels, cell proliferation and resistance to chemotherapy, and these phenomena could be reversed by TLR4 gene knockdown. Similarly, LPS stimulation of human liver cancer cell line H7402 resulted in TLR4 upregulation, NF-κB activation, TNF, IL-6 and IL-8 production and increased proliferation that could be reversed by signal transducer and STAT3 inhibition.Besides the well known successful usage of Bacillus Calmette–Guérin (BCG) in the therapy of bladder cancer there

neg: Hepatitis B particular virus-specific cytotoxic T lymphocytes(CTLs), contributes to most of the liver injury associated with HBV infection. CTLs eliminate HBV infection by killing infected cells and producing antiviral cytokines, which are then used to purge HBV from viable hepatocytes. Although liver damage is initiated and mediated by the CTLs, antigen-nonspecific inflammatory cells can worsen CTL-induced immunopathology, and platelets activated at the site of infection may facilitate the accumulation of CTLs in the liver. The tests, called assays, for detection of virus infection involve serum or blood tests that detect either viral antigens (proteins produced by the virus) or antibodies produced by

neg: Toxoplasma gondii an uninfected host consumes a tissue cyst, bradyzoites released from the cyst infect intestinal epithelial cells before converting to the proliferative tachyzoite stage. Following the initial period of proliferation throughout the host body, tachyzoites then convert back to bradyzoites, which reproduce inside host cells to form tissue cysts in the new host. Sporozoites are the stage of the parasite residing within oocysts. When a human or other warm-blooded host consumes an oocyst, sporozoites are released from it, infecting epithelial cells before converting to the proliferative tachyzoite stage. Initially, a "T. gondii" infection stimulates production of IL-2 and IFN-γ by the

neg: Glucocorticoid therefore, blunts the capacity of the immune system to mount a response. Glucocorticoids suppress cell-mediated immunity by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and IFN-γ, the most important of which is IL-2. Smaller cytokine production reduces the T cell proliferation. Glucocorticoids, however, not only reduce T cell proliferation, but also lead to another well known effect - glucocorticoid-induced apoptosis. The effect is more prominent in immature T cells still inside in the thymus, but peripheral T cells are also affected. The exact mechanism regulating this glucocorticoid sensitivity lies in the Bcl-2 gene.

neg: Toxoplasma gondii study of >1600 individuals found that Toxoplasma infection was especially common among people who expressed certain MHC alleles (HLA-B*08:01,HLA-C*04:01, HLA-DRB 03:01, HLA-DQA*05:01 and HLA-DQB*02:01). IL-12 is produced during "T. gondii" infection to activate natural killer (NK) cells. Tryptophan is an essential amino acid for "T. gondii," which it scavenges from host cells. IFN-γ induces the activation of indole-amine-2,3-dioxygenase (IDO) and tryptophan-2,3-dioxygenase (TDO), two enzymes that are responsible for the degradation of tryptophan. Immune pressure eventually leads the parasite to form cysts that normally are deposited in the muscles and in the brain of the hosts. The IFN-γ-mediated activation of IDO

neg: Ocular immune system to bacteria, aiding in their detection via other pathways. Corneal epithelial cells present a physical barrier to prevent microbes from reaching the interior of the eye chamber, which is effectively separated from the rest of the body via tight junctions. At the same time, corneal epithelial cells also secrete cytokines to activate microbial defense. One cytokine, interleukin (IL)-1α, is stored in epithelial cells and automatically released when the cell membrane is ruptured by infection or trauma. However, long-term effects of IL-1α can lead to not only enhanced immune infiltration of the cornea, but also neovascularization (formation of new blood vessels),

neg: Nasal-associated lymphoid tissue NALT is inductive site of MALT similarly to Peyer's patches in a small intestine. After intranasal immunization or pathogen recognition, lymphocytes in NALT proliferate and differentiate. They start to produce cytokines, such as IFN-γ, type I interferons, IL-2, IL-4, IL-5, IL-6 or IL-10 (amount depend on used immunizating agent or adjuvans). B cells go through isotype switching and produce antigen-specific IgM, IgG and mainly IgA. Activated B cells can migrate through body to respiratory and genito-uritary tract, because they express chemokine receptors CCR10 and αβ-integrin. Memory T and B cells are established and last for long time after immunization. Intranasal

neg: GNLY expression of a number of cytokines, including RANTES, MCP-1, MCP-3, MIP-1α, IL-10, IL-1, IL-6 and IFNα. Mice do not have a granulysin homolog, but transgenic mice expressing human granulysin have been engineered. Granulysin has been implicated in a myriad of diseases including infection, cancer, transplantation, autoimmunity, skin and reproductive maladies. GNLY Granulysin, also known as GNLY, is a protein which in humans is encoded by the "GNLY" gene. Granulysin is a protein present in cytotoxic granules of cytotoxic T cells and natural killer cells. Granulysin is a member of the saposin-like protein (SAPLIP) family and is released from cytotoxic T

neg: Immunosuppressive drug on lymphocyte subpopulations in tissues using immunohistochemistry. Immunosuppressive drugs can be classified into five groups: In pharmacologic (supraphysiologic) doses, glucocorticoids, such as prednisone, dexamethasone, and hydrocortisone are used to suppress various allergic, inflammatory, and autoimmune disorders. They are also administered as posttransplantory immunosuppressants to prevent the acute transplant rejection and graft-versus-host disease. Nevertheless, they do not prevent an infection and also inhibit later reparative processes. Glucocorticoids suppress the cell-mediated immunity. They act by inhibiting genes that code for the cytokines Interleukin 1 (IL-1), IL-2, IL-3, IL-4, IL-5, IL-6, IL-8, and TNF-alpha, the most important of which is IL-2. Smaller cytokine

neg: Uveitis cells produce large amounts of TGF beta and other suppressive cytokines, including IL-10, to prevent damage to the eye by reducing inflammation and causing T cells to differentiate to inducible T reg cells. Innate immune stimulation by bacteria and cellular stress is normally suppressed by myeloid suppression while inducible Treg cells prevent activation and clonal expansion of the autoreactive Th1 and Th17 cells that possess potential to cause damage to the eye. Whether through infection or other causes, this balance can be upset and autoreactive T cells allowed to proliferate and migrate to the eye. Upon entry to the eye,

neg: Anaplasma phagocytophilum cells. This bacterium has the ability to affect neutrophils by altering the function of the host cell. It can survive the first encounter with the host cell by detoxifying superoxide produced by neutrophil phagocyte oxidase assembly. It also disrupts normal neutrophil function, such as endothelial cell adhesion, transmigration, motility, degranulation, respiratory burst, and phagocytosis. It causes an increase in the secretion of IL-8, a chemoattractant that increases the phagocytosis of neutrophils. The purpose of this is to increase bacterial dissemination into the neutrophil. These tests can be performed to determine an "A. phagocytophilum" infection: Patients suffering from human granulocytic anaplasmosis

neg: Interleukin 27 express IL-17, IL-22, and granulocyte macrophage colony-stimulating factor (GM-CSF), are inhibited by IL-27 through STAT1 and expression of transcription factor RORγt. Tr1 cells, which express IL-10, are induced by IL-27 through the transcription factor c-Maf. Treg cells are inhibited by IL-27 through STAT1 and STAT3. IL-10 acts in an anti-inflammatory manner by suppressing inflammatory responses. One way that IL-27 can have an anti-inflammatory response is through the expression of IL-10. IL-27 has been found to be involved in the production of IL-10 by stimulating the various subsets of T cells, especially Tr1 cells. Also involved are the STAT1 and STAT3

neg: Toll-like receptor 11 mice) did not mount the IL-12 response upon profilin stimulation. Dendritic cells in the knock-out mice also failed to migrate to lymph nodes, halting the initiation of the adaptive immune response. Furthermore, mice lacking the "TLR 11" gene are susceptible to pancreatitis, fat cell necrosis, and increased inflammatory reactants. Pancreatitis is also a pathological response in humans to T. gondii infection. Wild-type mice are able to produce an immune response, marked by IL-12 and IFN-gamma production that is unseen in humans, who lack a functional TLR 11 protein. Uropathogenic "E. coli" is a bacterium that causes urinary tract infections. The

neg: Vogt–Koyanagi–Harada disease lead to granulomatous anterior inflammation, cataracts, glaucoma and ocular hypertension. Full-blown recurrences are, however, rare after the acute stage is over. Dysacusia may occur in this phase. Although there is sometimes a preceding viral infection, or skin or eye trauma, the exact underlying initiator of VKH disease remains unknown. However, VKH is attributed to aberrant T-cell-mediated immune response directed against self-antigens found on melanocytes. Stimulated by interleukin 23 (IL-23), T helper 17 cells and cytokines such as interleukin 17 (IL-17) appear to target proteins in the melanocyte. Affected individuals are typically 20 to 50 years old. The female to male

neg: Allergic bronchopulmonary aspergillosis to continue evading host responses, notably the use of proteolytic enzymes that interrupt IgG antibodies aimed towards it. Another important feature is its ability to interact and integrate with epithelial surfaces, which results in massive pro-inflammatory counter-response by the immune system involving IL-6, IL-8 and MCP-1 (a CCL2 receptor ligand). Proteases released by both the fungus and neutrophils induce further injury to the respiratory epithelium, leading to initiation of repair mechanisms (such as influx of serum and extracellular matrix (ECM) proteins) at the site of infection. Aspergillus spores and hyphae can interact with ECM proteins, and it is hypothesised that

neg: Pyroptosis and IL-18. The cytokines, once processed, will be in their biologically active form ready to be released from the host cells. The development of efficient adaptive immune responses depends on the recruitment and activation of the immune cells by inflammatory cytokines. Pyroptosis acts as a defence mechanism against infection by inducing pathological inflammation. The formation of inflammasomes and the activity of caspase-1 determine the balance between pathogen resolution and disease. In a healthy cell, caspase-1 activation helps to fight infection caused by "Salmonella" and "Shigella" via introducing cell death to restrict pathogen growth. When the ‘danger' signal is sensed, the

neg: Treg17 cells IL-23 and IL-6 are pathogenic upon adoptive transfer in type 1 diabetes while cells polarized with TGF-beta and IL-6 are not pathogenic., The intracellular aryl hydrocarbon receptor (AhR), which is activated by certain aromatic compounds, is specifically expressed in Treg17 cells. These cells are regulated by IL-23 and TGF-beta. The production of IL-22 in this subset of Th17 cells is regulated by AhR and Treg17 cells are depend on activation of the transcription factor Stat3. In a steady state, TGF-beta and AhR ligands induce low expression of IL-22 along with high expression of AhR, c-MAF, IL-10, and IL-21 that might

neg: Gluten immunochemistry such as viral infection. In addition, other cytokines such as IL12 and IL2, which are typically associated with T-helper cell stimulation, are not involved. In these two ways the innate peptide activation of T-cells in celiac disease is strange. IL-15 appears to induce increases in MICA and NKG2D that may increase brush-border cell killing. In addition, innate immunity to IRP peptide is involved in coeliac disease, dermatitis herpetiformis and possibly juvenile diabetes. IRP targets monocytes and increases the production of IL-15 by an HLA-DQ "independent" pathway, a subsequent study showed that both this region and the "33mer" could create the

neg: Pyroptosis quiescent cells will be activated to undergo pyroptosis and produce inflammatory cytokines IL-1β and IL-18. IL-18 will stimulate IFNγ production and initiates the development of T1 responses. (T1 responses tend to release cytokines that direct an immediate removal of the pathogen). The cell activation results in an increase in cytokine levels, which will augment the consequences of inflammation and this, in turn, contributes to the development of the adaptive response as infection progresses. The ultimate resolution will clear pathogens. In contrast, persistent inflammation will produce excessive immune cells which will be detrimental. If the amplification cycles persist, metabolic disorder, autoinflammatory