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Cytotoxic T cell

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370: 171: 725:. This strongly suggests that rheumatoid arthritis is caused by unidentified arthritogenic antigens. The antigen could be any exogenous antigen, such as viral proteins, or an endogenous protein. Recently, a number of possible endogenous antigens have been identified, for example, human cartilage glycoprotein 39, heavy chain binding protein and citrullinated protein. Activated CD4+ T lymphocytes stimulate monocytes, macrophages and synovial fibroblasts to elaborate the cytokines 38: 807: 2342: 260:, in which those double-positive T cells that bind to foreign antigen in the presence of self MHC. They will differentiate into either CD4 or CD8 depending on which MHC is associated with the antigen presented (MHC1 for CD8, MHC2 for CD4). In this case, the cells would have been presented antigen in the context of MHC1. Positive selection means selecting those TCRs capable of recognizing self MHC molecules. 316: 379:
that have been in contact with the antigen at least once but have returned subsequently to a quiescent or inactive state, ready to respond again to the antigen against which they were stimulated. Finally, when the specific immune response is triggered, these naive and memory T cells are activated, giving rise to effector T cells that have the capacity to kill pathogens or tumor cells.
721:, increased vascularity and infiltration of inflammatory cells; mainly CD4+ T lymphocytes, which are the main organisers of cell-mediated immune responses. In different studies, rheumatoid arthritis is strongly linked to major histocompatibility complex (MHC) class II antigens. The only cells in the body that express MHC class II antigens are constitutive 227:), which recognize non-protein antigens. The latter are characterised by their ability to recognise antigens that are not presented. In addition, they can recognise microbial toxic shock proteins and self-cell stress proteins. T γδ cells possess a wide functional plasticity after recognising infected or transformed cells, as they are able to produce 390:). In the thymus-independent pathway, because the APC is infected, it is highly activated and expresses a large number of co-receptors for coactivation. If APCs are not infected, CD4 cells need to be involved: either to activate the APC by co-stimulation (more common) or to directly activate the Tc cell by secreting 651:(DNA-activated protein kinase). The final result is apoptosis of the cell that expressed Fas. CD8 T cells can also show Activation Induced Cell Death or AICD which is mediated by CD3 receptor complex. Recently, a platelet released protein TLT-1 has been shown to induce AICD like cell death in CD8 T cells 638:
effector cells. Engagement of Fas with FasL allows for recruitment of the death-induced signaling complex (DISC). The Fas-associated death domain (FADD) translocates with the DISC, allowing recruitment of procaspases 8 and 10. These caspases then activate the effector caspases 3, 6, and 7, leading to
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The immune system must recognize millions of potential antigens. There are fewer than 30,000 genes in the human body, so it is impossible to have one gene for every antigen. Instead, the DNA in millions of white blood cells in the bone marrow is shuffled to create cells with unique receptors, each of
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is suggested to play a key role in CD8 T cell function, acting as a regulatory gene in the adaptive immune response. Studies investigating the effect of loss-of-function Eomesodermin found that a decrease in expression of this transcription factor resulted in decreased amount of perforin produced by
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T cells go through different stages, depending on the number of times they have been in contact with the antigen. In the first place, naĂŻve T-lymphocytes are those cells that have not yet encountered an antigen in the thymus. Then, T-lymphocytes become memory T cells. This type of T cells are those
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Only those T cells that bind to the MHC-self-antigen complexes weakly are positively selected. Those cells that survive positive and negative selection differentiate into single-positive T cells (either CD4 or CD8), depending on whether their TCR recognizes an MHC class I-presented antigen (CD8) or
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activation through immune complex formation. Moreover, several animal studies suggest that cytotoxic T cells may have a predominantly proinflammatory effect in the disease. It is also studied that the production of cytokines by the CD8+ cells may accelerate the progresses of the arthritis disease.
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DNA to form a developmental form of the TCR protein, known as pre-TCR. If that rearrangement is successful, the cells then rearrange their alpha-chain TCR DNA to create a functional alpha-beta TCR complex. This highly-variable genetic rearrangement product in the TCR genes helps create millions of
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infection. HIV over time has developed many strategies to evade the host cell immune system. For example, HIV has adopted very high mutation rates to allow them to escape recognition by CD8 T cells. They are also able to down-regulate expression of surface MHC Class I proteins of cells that they
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and CD8 T cells. During this process, the CD4 helper T cells "license" the dendritic cells to give a potent activating signal to the naive CD8 T cells. This licensing of antigen-presenting cells by the CD4 T helper cells proceeds by signaling between CD154/CD40L on the T helper cell and the CD40
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In this immunofluorescence image, a group of killer T cells (outer three) is engaging a cancer cell (centered one). A patch of signaling molecules (pink) that gathers at the site of cell-cell contact indicates that the CTL has identified a target. Lytic granules (red) that contain cytotoxic
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If activation occurs, the lymphocyte polarizes its granules towards the site of the synapse and releases them, producing a "lethal hit". At this point, it separates from the target cell, and can move on to another, and another. The target cell dies in about 6 hours, usually by apoptosis.
737:(TNFa), and to secrete metalloproteinases. The first three of which are key in driving inflammation in rheumatoid arthritis. These activated lymphocytes also stimulate B cells to produce immunoglobulins, including rheumatoid factor. Their pathogenic role is unknown, but may be due to 545:
While in most cases activation is dependent on TCR recognition of antigen, alternative pathways for activation have been described. For example, cytotoxic T cells have been shown to become activated when targeted by other CD8 T cells leading to tolerization of the latter.
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Helper T cells/CD4+ •express CD4 glycoproteins on their cell surface, which activate in the presence of peptide antigens on the surface of invading pathogens; •respond immediately to protect the immune system; •secrete different cytokine proteins according to the immune
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molecules, and brought to the surface of the cell by the class I MHC molecule, where they can be recognized by the T cell. If the TCR is specific for that antigen, it binds to the complex of the class I MHC molecule and the antigen, and the T cell destroys the cell.
686:(HBV) infection, cytotoxic T cells kill infected cells and produce antiviral cytokines capable of purging HBV from viable hepatocytes. They also play an important pathogenic role, contributing to nearly all of the liver injury associated with HBV infection. 179:
which can bind to a different antigen. Some receptors bind to tissues in the human body itself, so to prevent the body from attacking itself, those self-reactive white blood cells are destroyed during further development in the
235:(IP-10, lymphotactin), trigger cytolysis of target cells (perforins, granzymes...), and interact with other cells, such as epithelial cells, monocytes, dendritic cells, neutrophils and B cells. In some infections, such as 601:(programmed cell death). This is called a "lethal hit” and allows to observe a wave-like death of the target cells. Due to high lipid order and negatively charged phosphatidylserine present in their plasma membrane, T 761:. However, CD8+ cells have been shown to play an effector role, responsible for the ultimate destruction of islet beta cells. However, in studies with NOD mice carrying a null mutation at the 253:
and are therefore termed "double-positive" (DP) T cells (CD4CD8). The double-positive T cells are exposed to a wide variety of self-antigens in the thymus and undergo two selection criteria:
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infect, in order to further evade destruction by CD8 T cells. If CD8 T cells cannot find, recognize and bind to infected cells, the virus will not be destroyed and will continue to grow.
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Pearce EL, Mullen AC, Martins GA, Krawczyk CM, Hutchins AS, Zediak VP, et al. (November 2003). "Control of effector CD8+ T cell function by the transcription factor Eomesodermin".
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cells once they become activated and are generally classified as having a pre-defined cytotoxic role within the immune system. However, CD8 T cells also have the ability to make some
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The activation of cytotoxic T cells is dependent on several simultaneous interactions between molecules expressed on the surface of the T cell and molecules on the surface of the
779:(cytotoxic T-lymphocytes attack the new organ after detecting it as foreign, due to HLA variation between donor and recipient); in excessive cytokine production in severe 2465: 239:, there is a clonal expansion of peripheral γδ T cells that have specific TCRs, indicating the adaptive nature of the immune response mediated by these cells. 561:
factor for T cells. This increases the number of cells specific for the target antigen that can then travel throughout the body in search of antigen-positive
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levels facilitated the recruitment of intrahepatic CXCR5+CD8+T cells and, these types of cells produced high levels of HBV-specific interferon (IFN)-Îł and
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have been shown to facilitate the accumulation of virus-specific cytotoxic T cells into the infected liver. In some studies with mice, the injection with
626:(Apo1)(CD95) molecules expressed on the target cell. However, this Fas-Fas ligand interaction is thought to be more important to the disposal of unwanted 2749: 830: 1285:
Bennett SR, Carbone FR, Karamalis F, Flavell RA, Miller JF, Heath WR (June 1998). "Help for cytotoxic-T-cell responses is mediated by CD40 signalling".
765:(B2M) locus and thus lacking major histocompatibility complex class I molecules and CD8+ T cells, it was found that they did not develop diabetes. 1187: 2010:
Wang B, Gonzalez A, Benoist C, Mathis D (August 1996). "The role of CD8+ T cells in the initiation of insulin-dependent diabetes mellitus".
772:(CIPN). Mice without CD8 T cells show prolonged CIPN compared to normal mice and injection of educated CD8 T cells resolve or prevent CIPN. 769: 757:. Studies in a diabetic mouse model showed that CD4+ cells are responsible for the massive infiltration of mononuclear leukocytes into 382:
The threshold for activation of these cells is very high, and the process can occur via two pathways: thymus-independent (by infected
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TCRs have two parts, usually an alpha and a beta chain. (Some TCRs have a gamma and a delta chain. They are inherent to act against
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Wiebe C, Nickerson PW (February 2020). "Human leukocyte antigen molecular mismatch to risk stratify kidney transplant recipients".
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A simple activation of naive CD8 T cells requires the interaction with professional antigen-presenting cells, mainly with matured
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cells, cells that are infected by intracellular pathogens (such as viruses or bacteria), or cells that are damaged in other ways.
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components then travel along the microtubule cytoskeleton (green) to the contact site and are secreted, thus killing the target.
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Neumann H, Medana IM, Bauer J, Lassmann H (June 2002). "Cytotoxic T lymphocytes in autoimmune and degenerative CNS diseases".
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Carvalheiro H, da Silva JA, Souto-Carneiro MM (January 2013). "Potential roles for CD8(+) T cells in rheumatoid arthritis".
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Kabelitz D, Wesch D (2003). "Features and functions of gamma delta T lymphocytes: focus on chemokines and their receptors".
295: 2598: 1105:"Concurrent interaction of DCs with CD4(+) and CD8(+) T cells improves secondary CTL expansion: It takes three to tango" 2735: 2346: 2352: 223:
express alpha-beta TCRs (αβ T cells), but some T cells in epithelial tissues (like the gut) express gamma-delta TCRs (
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are generated, damaging the subject); inflammatory and degenerative diseases of the central nervous system, such as
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and to allow repetitive stimulation of cytotoxic T cells, dendritic cells have to interact with both, activated CD4
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Iannacone M, Sitia G, Guidotti LG (2006). "Pathogenetic and antiviral immune responses against hepatitis B virus".
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cell and the target cell bound closely together during antigen-specific activation. CD8 T cells are recognized as T
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Cytotoxic T-lymphocytes have been implicated in the development of various diseases and disorders, for example in
3076: 3019: 2557: 1759:"CXCL13-mediated recruitment of intrahepatic CXCR5CD8 T cells favors viral control in chronic HBV infection" 2679: 2649: 2629: 2055:"Cisplatin educates CD8+ T cells to prevent and resolve chemotherapy-induced peripheral neuropathy in mice" 1201:
Hivroz C, Chemin K, Tourret M, Bohineust A (2012). "Crosstalk between T lymphocytes and dendritic cells".
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Hoyer S, Prommersberger S, Pfeiffer IA, Schuler-Thurner B, Schuler G, Dörrie J, Schaft N (December 2014).
1016:"Characterization of Adaptive-like γδ T Cells in Ugandan Infants during Primary Cytomegalovirus Infection" 2667: 2662: 2502: 2198:"Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology" 2104:"CD8+ T Cells and Endogenous IL-10 Are Required for Resolution of Chemotherapy-Induced Neuropathic Pain" 2905: 644: 558: 131:, which binds to the constant portion of the class I MHC molecule. Therefore, these T cells are called 2247:"COVID-19, cytokines and immunosuppression: what can we learn from severe acute respiratory syndrome?" 2245:
Sarzi-Puttini P, Giorgi V, Sirotti S, Marotto D, Ardizzone S, Rizzardini G, et al. (March 2020).
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Iannacone M, Sitia G, Isogawa M, Marchese P, Castro MG, Lowenstein PR, et al. (November 2005).
1387:"Preparing the lethal hit: interplay between exo- and endocytic pathways in cytotoxic T lymphocytes" 1338:"CTLs respond with activation and granule secretion when serving as targets for T-cell recognition" 1014:
Tuengel J, Ranchal S, Maslova A, Aulakh G, Papadopoulou M, Drissler S, et al. (October 2021).
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Chang HF, Bzeih H, Chitirala P, Ravichandran K, Sleiman M, Krause E, et al. (February 2017).
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different T cells with different TCRs, helping the body's immune system respond to virtually any
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Rudd-Schmidt JA, Hodel AW, Noori T, Lopez JA, Cho HJ, Verschoor S, et al. (November 2019).
3107: 2825: 2761: 2549: 967:"Ligand recognition by the γδ TCR and discrimination between homeostasis and stress conditions" 2102:
Krukowski K, Eijkelkamp N, Laumet G, Hack CE, Li Y, Dougherty PM, et al. (October 2016).
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Gulzar N, Copeland KF (January 2004). "CD8+ T-cells: function and response to HIV infection".
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In order for the TCR to bind to the class I MHC molecule, the former must be accompanied by a
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Milstein O, Hagin D, Lask A, Reich-Zeliger S, Shezen E, Ophir E, et al. (January 2011).
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for T cell activation. This second signal can be assisted (or replaced) by stimulating the T
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Tsai S, Shameli A, Santamaria P (2008). "Chapter 4 CD8+ T Cells in Type 1 Diabetes".
1951: 1913: 1878: 1839: 1792: 1780: 1739: 1663: 1606: 1560: 1507: 1473: 1416: 1367: 1310: 1267: 1218: 1214: 1169: 1159: 1126: 1082: 1072: 1047: 996: 947: 912: 877: 863: 758: 738: 714: 683: 298:-presented antigen (CD4). It is the CD8 T-cells that will mature and go on to become 170: 2323: 2070: 2039: 1851: 1618: 3178: 3119: 3059: 3031: 3026: 2994: 2981: 2971: 2517: 2303: 2258: 2217: 2209: 2162: 2125: 2120: 2115: 2074: 2066: 2019: 1974: 1943: 1905: 1829: 1819: 1770: 1729: 1721: 1690: 1653: 1645: 1598: 1550: 1540: 1499: 1463: 1455: 1406: 1398: 1357: 1349: 1322: 1302: 1257: 1210: 1138: 1116: 1037: 1027: 986: 978: 939: 904: 855: 191: 159: 89: 41:
Antigen presentation stimulates T cells to become either "cytotoxic" CD8+ cells or
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receptor on the antigen-presenting cell during immunological synapse formation.
530: 468: 425: 211: 108: 100: 3041: 2986: 2927: 2847: 2820: 1824: 1775: 1758: 1529:"Platelet-derived TLT-1 promotes tumor progression by suppressing CD8+ T cells" 1459: 812: 703: 538: 534: 511: 402: 2213: 1402: 1086: 982: 908: 608:
A second way to induce apoptosis is via cell-surface interaction between the T
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cells are resistant to the effects of their perforin and granzyme cytotoxins.
3172: 3009: 2898: 2716: 2698: 2536: 2498: 2419: 1947: 1694: 1173: 825: 730: 713:. The main involvement of rheumatoid arthritis is its joint involvement. The 627: 554: 520: 414: 391: 387: 42: 1602: 2976: 2961: 2956: 2893: 2791: 2531: 2439: 2434: 2315: 2272: 2231: 2174: 2139: 2088: 2023: 1996: 1955: 1917: 1882: 1866: 1843: 1784: 1743: 1667: 1610: 1564: 1477: 1420: 1371: 1222: 1130: 1066: 1051: 1000: 951: 916: 655: 622: 562: 410: 406: 286: 124: 112: 2031: 1808:"Antibody-dependent and -independent mechanisms of inflammatory arthritis" 1314: 1271: 1153: 1121: 1104: 1102: 2711: 2414: 2409: 1545: 718: 597:
cascade, which is a series of cysteine proteases that eventually lead to
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infection (due to an exaggerated lymphocyte response, a large amount of
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1436:"Lipid order and charge protect killer T cells from accidental death" 710: 687: 598: 582: 282: 232: 679:
infections, cytotoxic T cells are mostly effective against viruses.
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coreceptor and the class I MHC molecule to stabilize this signal.
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Advanced Hematology in Integrated Cardiovascular Chinese Medicine
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during their development or to the lytic activity of certain T
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cell undergoes clonal expansion with the help of the cytokine
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following their activation with a class I-restricted antigen.
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Cytotoxic T cells have been implicated in the progression of
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because they could otherwise become autoreactive, leading to
1200: 2052: 1580: 1433: 1013: 503: 499: 492: 2293: 1973:. Advances in Immunology. Vol. 100. pp. 79–124. 1098: 1096: 2009: 746: 481: 247: 243: 128: 1864: 791:(T cells become sensitised to certain proteins, such as 1631: 1093: 573:
When exposed to infected/dysfunctional somatic cells, T
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T cells with functionally stable TCRs express both the
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Cope AP, Schulze-Koops H, Aringer M (September 2007).
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Kemball CC, Alirezaei M, Whitton JL (September 2010).
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is activated it starts to express the surface protein
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T cell that kills infected, damaged or cancerous cells
2195: 1968: 1867:"The central role of T cells in rheumatoid arthritis" 107:. An antigen is a molecule capable of stimulating an 802: 174:
Development of single positive T cells in the thymus
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List of distinct cell types in the adult human body
266:, in which those double-positive T cells that bind 3170: 1489: 1487: 662: 634:cells than it is to the cytolytic activity of T 187:is necessary for its development and activity. 2152: 1971:Immunopathogenesis of Type 1 Diabetes Mellitus 1933: 1493: 1064: 894: 745:CD8 T cells have been found to play a role in 2743: 2373: 1805: 1756: 1484: 929: 162:, with antitumour and antimicrobial effects. 1625: 1329: 1235: 753:Furthermore, CD8 T cells may be involved in 337:. There might be a discussion about this on 142:between CD8 and the MHC molecule keeps the T 1229: 964: 888: 694:CD8+T cells show a significant decrease of 2750: 2736: 2380: 2366: 1186:: CS1 maint: location missing publisher ( 770:chemotherapy-induced peripheral neuropathy 480:There is a second interaction between the 194:and form part of the epithelial barrier). 2262: 2221: 2196:Channappanavar R, Perlman S (July 2017). 2129: 2119: 2078: 1833: 1823: 1774: 1733: 1657: 1554: 1544: 1467: 1410: 1361: 1261: 1120: 1041: 1031: 990: 420:, the cells degrade foreign proteins via 357:Learn how and when to remove this message 2155:Current Opinion in Organ Transplantation 1152:Abbas AK, Lichtman AH, Pillai S (2018). 849: 768:CD8 T cells may be necessary to resolve 620:(FasL)(Apo1L)(CD95L), which can bind to 368: 169: 36: 2620: 413:. When these cells are infected with a 14: 3171: 2251:Clinical and Experimental Rheumatology 1871:Clinical and Experimental Rheumatology 2731: 2361: 1929: 1927: 1576: 1574: 1526: 639:cleavage of death substrates such as 568: 103:(TCRs) that can recognize a specific 1806:Chang MH, Nigrovic PA (March 2019). 1391:Cellular and Molecular Life Sciences 1158:(Ninth ed.). Philadelphia, PA. 965:Deseke M, Prinz I (September 2020). 309: 219:of an invader. The vast majority of 2599:Mucosal associated invariant T cell 971:Cellular & Molecular Immunology 850:Al-Shura AN (2020). "Lymphocytes". 671:, which are effective against both 24: 1962: 1924: 1571: 1527:Tyagi, Tarun; et al. (2023). 1496:Encyclopedia of Medical Immunology 1278: 860:10.1016/b978-0-12-817572-9.00007-0 519:cell with cytokines released from 435:(APC). For instance, consider the 25: 3200: 2353:T-cell Group – Cardiff University 2334: 1155:Cellular and molecular immunology 944:10.1615/CritRevImmunol.v23.i56.10 2635:Lymphokine-activated killer cell 2340: 2264:10.55563/clinexprheumatol/xcdary 1533:Journal of Experimental Medicine 1215:10.1615/CritRevImmunol.v32.i2.30 805: 401:Class I MHC is expressed by all 314: 2387: 2287: 2238: 2189: 2146: 2095: 2071:10.1097/j.pain.0000000000001512 2046: 2003: 1889: 1858: 1799: 1750: 1701: 1674: 1520: 1427: 1378: 612:and the infected cell. When a T 99:Most cytotoxic T cells express 3077:Immunoglobulin class switching 2121:10.1523/JNEUROSCI.3708-15.2016 2012:European Journal of Immunology 1203:Critical Reviews in Immunology 1145: 1109:European Journal of Immunology 1058: 1007: 958: 932:Critical Reviews in Immunology 923: 557:(IL-2), which is a growth and 165: 13: 1: 2308:10.1016/S0166-2236(02)02154-9 1979:10.1016/S0065-2776(08)00804-3 1238:"Immunology. Licence to kill" 836: 577:cells release the cytotoxins 305: 2680:Type 3 innate lymphoid cells 2668:Type 2 innate lymphoid cells 2663:Type 1 innate lymphoid cells 2650:Uterine natural killer cells 2630:Cytokine-induced killer cell 2167:10.1097/MOT.0000000000000714 1910:10.1016/j.autrev.2012.07.011 1504:10.1007/978-0-387-84828-0_36 1354:10.1182/blood-2010-05-283770 1236:Lanzavecchia A (June 1998). 854:. Elsevier. pp. 41–46. 735:tumour necrosis factor alpha 663:Role in disease pathogenesis 643:, lamin B1, lamin B2, PARP ( 7: 2202:Seminars in Immunopathology 2108:The Journal of Neuroscience 798: 509:CD80 and CD86 are known as 506:(also called B7-1 and B7-2) 10: 3205: 2906:Polyclonal B cell response 1825:10.1172/jci.insight.125278 1776:10.1016/j.jhep.2019.09.031 1460:10.1038/s41467-019-13385-x 785:pro-inflammatory cytokines 645:poly ADP ribose polymerase 533:. To generate longlasting 386:) or thymus-dependent (by 231:(IFN-Îł, TNF-α, IL-17) and 29: 3140: 3098: 3040: 2941: 2871: 2779: 2772: 2697: 2658: 2611: 2579: 2483: 2474: 2395: 2214:10.1007/s00281-017-0629-x 1403:10.1007/s00018-016-2350-7 1065:Rojas-Espinosa O (2017). 983:10.1038/s41423-020-0503-y 909:10.1016/j.nut.2009.06.002 821:CTL-mediated cytotoxicity 654:The transcription factor 111:and is often produced by 1948:10.2174/1570162043485077 1695:10.2217/17460794.1.2.189 1068:InmunologĂ­a (de memoria) 723:antigen-presenting cells 196:Hematopoietic stem cells 30:Not to be confused with 2707:Hematopoietic stem cell 2466:Lymphoplasmacytoid cell 2296:Trends in Neurosciences 1603:10.1126/science.1090148 698:. Also, an increase of 433:antigen-presenting cell 426:T cell antigen receptor 3020:Tolerance in pregnancy 2762:adaptive immune system 2024:10.1002/eji.1830260815 593:function triggers the 495:molecule on the T cell 428:(TCR) on CD8 T cells. 405:cells, except for non- 375: 175: 62:cytotoxic T lymphocyte 46: 3055:Somatic hypermutation 2889:Polyclonal antibodies 2884:Monoclonal antibodies 2613:Innate lymphoid cells 2589:Natural killer T cell 1877:(5 Suppl 46): S4-11. 1763:Journal of Hepatology 1440:Nature Communications 1122:10.1002/eji.201444477 549:Once activated, the T 372: 237:human cytomegalovirus 206:, where they undergo 173: 40: 32:Natural killer T cell 3072:Junctional diversity 2840:Antigen presentation 2349:at Wikimedia Commons 1936:Current HIV Research 1898:Autoimmunity Reviews 1546:10.1084/jem.20212218 1498:. pp. 332–342. 777:transplant rejection 763:beta-2 microglobulin 717:is characterised by 327:confusing or unclear 210:of their beta-chain 3067:V(D)J recombination 3050:Affinity maturation 2802:Antigenic variation 2581:Innate-like T cells 2461:Transitional B cell 2114:(43): 11074–11083. 1638:Future Microbiology 1595:2003Sci...302.1041P 1589:(5647): 1041–1043. 1452:2019NatCo..10.5396R 1299:1998Natur.393..478B 1254:1998Natur.393..413L 335:clarify the section 225:gamma delta T cells 208:V(D)J recombination 43:"helper" CD4+ cells 1650:10.2217/fmb.10.101 789:multiple sclerosis 569:Effector functions 422:antigen processing 376: 264:negative selection 258:positive selection 176: 47: 3166: 3165: 3094: 3093: 2844:professional APCs 2725: 2724: 2693: 2692: 2607: 2606: 2347:Cytotoxic T cells 2345:Media related to 1720:(11): 1167–1169. 1513:978-0-387-84827-3 1293:(6684): 478–480. 1248:(6684): 413–414. 1165:978-0-323-52323-3 1115:(12): 3543–3559. 1078:978-968-7988-28-3 1033:10.3390/v13101987 869:978-0-12-817572-9 759:pancreatic islets 715:synovial membrane 684:hepatitis B virus 527: 526: 445:cell activation. 367: 366: 359: 300:cytotoxic T cells 202:migrate into the 16:(Redirected from 3196: 3060:Clonal selection 3032:Immune privilege 3027:Immunodeficiency 2982:Cross-reactivity 2972:Hypersensitivity 2777: 2776: 2752: 2745: 2738: 2729: 2728: 2645:Adaptive NK cell 2618: 2617: 2481: 2480: 2382: 2375: 2368: 2359: 2358: 2344: 2328: 2327: 2291: 2285: 2284: 2266: 2242: 2236: 2235: 2225: 2193: 2187: 2186: 2150: 2144: 2143: 2133: 2123: 2099: 2093: 2092: 2082: 2065:(6): 1459–1468. 2050: 2044: 2043: 2018:(8): 1762–1769. 2007: 2001: 2000: 1966: 1960: 1959: 1931: 1922: 1921: 1893: 1887: 1886: 1862: 1856: 1855: 1837: 1827: 1803: 1797: 1796: 1778: 1754: 1748: 1747: 1737: 1705: 1699: 1698: 1678: 1672: 1671: 1661: 1644:(9): 1329–1347. 1629: 1623: 1622: 1578: 1569: 1568: 1558: 1548: 1524: 1518: 1517: 1491: 1482: 1481: 1471: 1431: 1425: 1424: 1414: 1382: 1376: 1375: 1365: 1348:(3): 1042–1052. 1333: 1327: 1326: 1282: 1276: 1275: 1265: 1233: 1227: 1226: 1198: 1192: 1191: 1185: 1177: 1149: 1143: 1142: 1124: 1100: 1091: 1090: 1062: 1056: 1055: 1045: 1035: 1011: 1005: 1004: 994: 962: 956: 955: 938:(5–6): 339–370. 927: 921: 920: 892: 886: 885: 847: 815: 810: 809: 448: 447: 438:two signal model 362: 355: 351: 348: 342: 318: 317: 310: 101:T-cell receptors 90:white blood cell 74:cytolytic T cell 51:cytotoxic T cell 21: 3204: 3203: 3199: 3198: 3197: 3195: 3194: 3193: 3169: 3168: 3167: 3162: 3136: 3090: 3036: 3015:Clonal deletion 2943: 2937: 2867: 2768: 2756: 2726: 2721: 2689: 2654: 2603: 2575: 2569: 2561: 2553: 2545: 2521: 2513: 2506: 2470: 2448: 2391: 2386: 2337: 2332: 2331: 2292: 2288: 2243: 2239: 2194: 2190: 2151: 2147: 2100: 2096: 2051: 2047: 2008: 2004: 1989: 1967: 1963: 1932: 1925: 1894: 1890: 1863: 1859: 1804: 1800: 1755: 1751: 1714:Nature Medicine 1706: 1702: 1683:Future Virology 1679: 1675: 1630: 1626: 1579: 1572: 1525: 1521: 1514: 1492: 1485: 1432: 1428: 1383: 1379: 1334: 1330: 1283: 1279: 1234: 1230: 1199: 1195: 1179: 1178: 1166: 1150: 1146: 1101: 1094: 1079: 1063: 1059: 1012: 1008: 963: 959: 928: 924: 893: 889: 870: 848: 844: 839: 811: 804: 801: 755:Type 1 diabetes 665: 637: 633: 615: 611: 604: 591:serine protease 576: 571: 559:differentiation 552: 531:dendritic cells 518: 444: 363: 352: 346: 343: 332: 319: 315: 308: 168: 149: 145: 109:immune response 58: 53:(also known as 35: 28: 23: 22: 15: 12: 11: 5: 3202: 3192: 3191: 3186: 3181: 3164: 3163: 3161: 3160: 3155: 3150: 3144: 3142: 3138: 3137: 3135: 3134: 3129: 3128: 3127: 3117: 3116: 3115: 3104: 3102: 3096: 3095: 3092: 3091: 3089: 3088: 3079: 3074: 3069: 3064: 3063: 3062: 3057: 3046: 3044: 3042:Immunogenetics 3038: 3037: 3035: 3034: 3029: 3024: 3023: 3022: 3017: 3012: 3007: 3002: 2990: 2989: 2987:Co-stimulation 2984: 2979: 2974: 2969: 2964: 2959: 2954: 2947: 2945: 2939: 2938: 2936: 2935: 2930: 2928:Immune complex 2924: 2923: 2918: 2913: 2908: 2903: 2902: 2901: 2896: 2891: 2886: 2875: 2873: 2869: 2868: 2866: 2865: 2860: 2855: 2850: 2848:Dendritic cell 2836: 2835: 2830: 2829: 2828: 2826:Conformational 2823: 2812: 2811: 2806: 2805: 2804: 2799: 2794: 2783: 2781: 2774: 2770: 2769: 2755: 2754: 2747: 2740: 2732: 2723: 2722: 2720: 2719: 2714: 2709: 2703: 2701: 2695: 2694: 2691: 2690: 2688: 2687: 2682: 2677: 2676: 2675: 2665: 2659: 2656: 2655: 2653: 2652: 2647: 2642: 2637: 2632: 2626: 2624: 2615: 2609: 2608: 2605: 2604: 2602: 2601: 2596: 2591: 2585: 2583: 2577: 2576: 2574: 2573: 2572: 2571: 2567: 2563: 2559: 2555: 2551: 2547: 2543: 2534: 2529: 2519: 2511: 2504: 2496: 2490: 2484: 2478: 2472: 2471: 2469: 2468: 2463: 2458: 2457: 2456: 2446: 2442: 2437: 2432: 2427: 2422: 2417: 2412: 2407: 2401: 2399: 2393: 2392: 2385: 2384: 2377: 2370: 2362: 2356: 2355: 2350: 2336: 2335:External links 2333: 2330: 2329: 2302:(6): 313–319. 2286: 2257:(2): 337–342. 2237: 2208:(5): 529–539. 2188: 2145: 2094: 2045: 2002: 1987: 1961: 1923: 1904:(3): 401–409. 1888: 1857: 1818:(5): e125278. 1798: 1769:(3): 420–430. 1749: 1726:10.1038/nm1317 1700: 1673: 1624: 1570: 1519: 1512: 1483: 1426: 1397:(3): 399–408. 1377: 1328: 1277: 1228: 1209:(2): 139–155. 1193: 1164: 1144: 1092: 1077: 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2494:Cytotoxic CD8 2491: 2489: 2486: 2485: 2482: 2479: 2477: 2473: 2467: 2464: 2462: 2459: 2455: 2452: 2451: 2450: 2443: 2441: 2438: 2436: 2433: 2431: 2430:Marginal zone 2428: 2426: 2423: 2421: 2418: 2416: 2413: 2411: 2408: 2406: 2403: 2402: 2400: 2398: 2394: 2390: 2383: 2378: 2376: 2371: 2369: 2364: 2363: 2360: 2354: 2351: 2348: 2343: 2339: 2338: 2325: 2321: 2317: 2313: 2309: 2305: 2301: 2297: 2290: 2282: 2278: 2274: 2270: 2265: 2260: 2256: 2252: 2248: 2241: 2233: 2229: 2224: 2219: 2215: 2211: 2207: 2203: 2199: 2192: 2184: 2180: 2176: 2172: 2168: 2164: 2160: 2156: 2149: 2141: 2137: 2132: 2127: 2122: 2117: 2113: 2109: 2105: 2098: 2090: 2086: 2081: 2076: 2072: 2068: 2064: 2060: 2056: 2049: 2041: 2037: 2033: 2029: 2025: 2021: 2017: 2013: 2006: 1998: 1994: 1990: 1988:9780123743268 1984: 1980: 1976: 1972: 1965: 1957: 1953: 1949: 1945: 1941: 1937: 1930: 1928: 1919: 1915: 1911: 1907: 1903: 1899: 1892: 1884: 1880: 1876: 1872: 1868: 1861: 1853: 1849: 1845: 1841: 1836: 1831: 1826: 1821: 1817: 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2425:Follicular 1087:1022564980 837:References 781:SARS-CoV-2 739:complement 669:antibodies 618:FAS ligand 587:granulysin 329:to readers 306:Activation 233:chemokines 154:, such as 78:CD8 T-cell 3158:Cytolysin 3148:Cytokines 2995:Tolerance 2944:tolerance 2863:Immunogen 2685:LTi cells 2640:Null cell 2488:Thymocyte 2281:214609305 2183:208537995 1793:204702318 1182:cite book 1174:973917896 897:Nutrition 883:response. 878:241913878 711:arthritis 688:Platelets 677:bacterial 599:apoptosis 583:granzymes 407:nucleated 283:apoptosis 229:cytokines 152:cytokines 3108:Cellular 2952:Immunity 2950:Action: 2933:Paratope 2921:Idiotype 2911:Allotype 2879:Antibody 2833:Mimotope 2797:Allergen 2780:Antigens 2773:Lymphoid 2673:Nuocytes 2622:NK cells 2454:B10 cell 2324:12593103 2316:12086750 2273:32202240 2232:28466096 2175:31789952 2140:27798187 2089:30720585 2040:26229701 1997:19111164 1956:15053338 1918:22841983 1883:17977483 1852:73512236 1844:30843881 1785:31610223 1744:16258538 1668:20860480 1619:43479181 1611:14605368 1565:36305874 1478:31776337 1421:27585956 1372:21045195 1223:23216612 1131:25211552 1052:34696417 1001:32709926 952:15030305 917:19647627 799:See also 649:DNA-PKcs 579:perforin 477:molecule 418:pathogen 281:undergo 278:antigens 140:affinity 3179:T cells 3153:Opsonin 3132:NK cell 3120:Humoral 3000:Central 2967:Allergy 2916:Isotype 2816:Epitope 2787:Antigen 2476:T cells 2405:B1 cell 2397:B cells 2223:7079893 2131:5098842 2080:6527475 2032:8765018 1835:6483516 1735:2908083 1659:3045535 1591:Bibcode 1583:Science 1556:9814191 1469:6881447 1448:Bibcode 1412:5241346 1363:3035066 1323:4325396 1315:9624004 1295:Bibcode 1272:9623994 1250:Bibcode 1139:5655814 1043:8537190 1020:Viruses 992:7608190 682:During 667:Unlike 647:), and 641:lamin A 595:caspase 498:either 325:may be 221:T cells 217:protein 198:in the 127:called 105:antigen 84:) is a 3125:B cell 3113:T cell 2858:B cell 2821:Linear 2809:Hapten 2420:Memory 2415:Plasma 2322:  2314:  2279:  2271:  2230:  2220:  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Index

CD8+
Natural killer T cell

"helper" CD4+ cells
T lymphocyte
white blood cell
cancer
T-cell receptors
antigen
immune response
cancer cells
class I MHC
glycoprotein
CD8
affinity
cytokines
TNF-α
IFN-Îł

thymus
iodine
stress
Hematopoietic stem cells
bone marrow
thymus
V(D)J recombination
TCR
protein
T cells
gamma delta T cells

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