The Role And Roles Of CD4 And C. T Cells

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CD4+ T lymphocytes, or cells, are white blood cells that are involved in immune protection. These cells assist B cells in creating antibodies, allow macrophages to establish heightened antimicrobial activity, recruit neutrophils, eosinophils, and basophils towards inflammation and infection. CD4+ T cells also produce a group of cytokines, which respectively, trigger an abundance of immune responses.
T cell differentiation Originally, Mosmann et al., 1986 reported that CD4 T cells can be subdivided into those that produce interferon gamma (IFN-ϒ) and those that produce interleukin 4 (IL-4). Currently, CD4 T cells are recognized as a cell population with a variety of functions. Two subsets of CD4+ T cells that are recognized individually are
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These T helper cells include Th1, Th2, and Th17. (Takeuchi et al., 2015) Mossoman et al., 1986 considered Th1 to be essential for intracellular microorganism immunity, and Th2 for extracellular pathogen immunity (Zhu et al., 2008). Th17’s roles were not yet discovered. Th1 is now known to be involved in cell-mediated immunity. T helper 1 (Th1) cells control intracellular pathogens, such as viruses and certain bacteria, by producing the cytokine IFN-ϒ. IFN-ϒ is called type II interferon; it’s a cytokine involved in regulating all phases of the inflammatory and immune responses. IFN-ϒ regulates the activation of both immune and inflammatory responses, Th1 activation, and growth & differentiation of T cells, B cells, macrophages, and natural killer cells. (Alvarez et al., 2005) Th1 is regulated by IFN-ϒ and interleukin 12 (IL-12). Interleukin 12 is a cytokine produced in response to intracellular pathogens and parasitic infection. It was discovered to be essential for the induction IFN-ϒ and for the activation of CD4+ cells. (Wolf et al., 1994) Th2 is involved in antibody-mediated responses against extracellular parasites, allergens, bacteria, and toxins. Th2 produces the cytokines: IL-4, IL-5, IL-9, and IL-13. (Takeuchi et al., 2015) IL-5 leads to eosinophils being recruited, while IL-4 and IL-13 cause an enhanced epithelial border to …show more content…
TSLC1 has the Necl-2 cell surface protein and it mediates epithelial cell junctions and makes sure the cells are growing in organized layers to ensure the inhibition of tumorigenesis. TSLC1 is often silenced in human lung carcinomas. NK cells and CD8+ T cells recognize Necl-2 through CRTAM, which is only expressed on activated NK and T cells. Interactions between CRTAM and Necl-2 increase the cytotoxicity of NK cells, the secretion of interferon- γ (IFN-γ) by CD8 + T cells, and NK cell-mediated killing of tumors that express Necl-2 in vivo. CRTAM’s presence may be responsible for signals that trigger the exocytosis of cytolytic granules. However, isolating the CRTAM-Necl-2 interaction did not yield significant IFN-γ release, which suggests that the interaction is not sufficient enough to trigger IFN-γ in NK cells and, therefore, might need other interactions to induce adequate cytokine production. (Boles et al.,

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