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Immunology - Essay Example

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T Helper Cells and the Adaptive Immune System Name Subject Instructor Institution Date T helper cells are a sub-group of lymphocytes, which is a type of white blood cells and plays an important role in the immune system majorly in the adaptive immune system…
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T Helper Cells and the Adaptive Immune System T helper cells are a sub-group of lymphocytes, which is a type of white blood cells and plays an important role in the immune system majorly in the adaptive immune system. They also play an important role in enabling activities of other immune cells in the body by releasing T cell cytokines which activates the other cells (Wan & Flavell, 2007). Other functions of T-helper cells in the body include facilitating the B cell antibody class switching, maximization of bactericidal activity of phagocytes, for example the macrophages as well as playing an important function in the growth and activation of cytotoxic T cells. As far as immunity of the human body is concerned, T-helper cells serve the most important function in adaptive immunity. They play a vital role in nearly all adaptive immune reactions. Apart from helping B cells secrete antibodies and assisting microphages destroy microbes that have been ingested, these cells also help in the activation of cytotoxic T Cells to help them kill infected target cells (Rang, H. P. 2003). These cells have a wide range of functions in the body, but they derive their name from the main role they play in the immune system. They serve an auxiliary function in the immune system by helping other effector cells to perform their functions effectively. Among the cells they help include cytotoxic T lymphocytes (CTLs) and B cells. The main help they provide to other cells in the immune system includes secreting cytokines which act as stimulators to activate the other cells. There are four main types of T-helper cells namely Th1, Th2, Tfh, and Th17. Each of them performs a specific role in the immune system (Hu, 2007). The Th1 for instance play essential functions in both antibody-mediated immunity and cell-mediated immunity. These cells are in the regulation of intracellular pathogens like viruses and certain types of bacteria such as Listeria and Mycobacterium tuberculosis which causes TB (Hu, 2007). Th1 cells provide cytokine-mediated assistance to cytotoxic t Lymphocytes, which are the most powerful cells against intracellular pathogens. Th2 T- helper cells are important in the production of LgE antibodies as well as production of other subclasses of lgG. They also offer their help to B Cells. The other type of T-helper cells, Tfh also provides help to B cells, assisting them to develop in to antibodies capable of secreting plasma cells in the nests of lymphoid cells also known as follicles located in the lymph nodes. These are the majority type of T-helper cells in the body and are commonly known as follicular helper T (Tfh) cells (Hirota et al, 2011). The Th17 T-helper cells on the other hand help in protection of other body surfaces such the skin and the lining of intestines from extracellular bacteria. In order to successfully perform their function, T-helper cells have to be activated so as to become effector cells. One of the most notable roles these cells play in adaptive immunity is in the role it plays in HIV infections. The HIV virus affects CD4+ cells in the human body. The virus kills all the CD4+ cells reducing their numbers and effectiveness. As a result, the patient’s immunity is inhibited and towards the end of the HIV infection, the patient suffers from Acquired immunodeficiency Syndrome (AIDS). Absence of CD4+ cells in the body also leads to other rare disorders that produce similar symptoms to AIDS but they are not as fatal as the AIDS. During the non symptomatic stage of HIV, the virus often has a high attraction for macrophages and a low one towards the T-Cells (Harrington et al, 2005). This results in a low skill rate for the CD4+ T cells in the immune system. This situation is initially resolved through production of other T helper cells from the thymus which originates from the bone marrow. When the virus becomes more lymphotropic and gets attracted to the T cells, it starts to infect the CD$+ T cells more efficiently as a result of a change in the co-receptors that it binds to in the course of the infection. This leads to the immune system being overwhelmed and the body becomes weaker and less resistant to diseases and other infections. The infection becomes more serious at this point when the CD4+ T cells get diminished and lose their efficiency in fighting against the antigens which could potentially be detected and killed. It is this lack of full antigen cover against immunity that results to the patient contracting Acquired Immunodeficiency Syndrome (AIDS). The depletion of CD4+ T cells during AIDS makes the body weaker and more susceptible to opportunistic infections which would normally require a response from helper T Cells so as to bypass the immune system of the patient. References Rang, H. P. (2003). Pharmacology. Edinburgh: Churchill Livingstone. Harrington, LE; Hatton, RD; Mangan, P. R. (2005), "Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages", Nature Immunology 6 (11): 1023–32, Hu, Wanchung (2007). Microarray analysis of PBMC gene expression profiles after Plasmodium falciparum malarial infection (Ph.D.). Johns Hopkins University Hirota K, Duarte JH, Veldhoen M, Hornsby E, Li Y, Cua DJ, Ahlfors H, Wilhelm C, Tolaini M, Menzel U, Garefalaki A, Potocnik AJ, Stockinger B. Nat Immunol (2011). "Fate mapping of IL-17-producing T cells in inflammatory responses". Nature Immunology 12 (3): 255–63. Larsen M, Arnaud L, Hie M, Parizot C, Dorgham K, Shoukry M, Kemula M, Barete S, Derai D, Sauce D, Amoura Z, Pene J, Yssel H, Gorochov G. Eur J Immunol (2011). "Multiparameter grouping delineates heterogeneous populations of human IL-17 and/or IL-22 T-cell producers that share antigen specificities with other T-cell subsets". European Journal of Immunology (UPMC Paris 06 Institut National de la Sante et de la Recherche Medicale (Inserm) UMR-S 945) 41 (9): 2596–2605 Nakayamada S., Takahashi H., Kanno Y., O'Shea J.J. (2012). "Helper T cell diversity and plasticity". Current Opinion in Immunology 24 (3): 297–302 Said E.A., Dupuy F.P., Trautmann L., Zhang Y., Shi Y., El-Far M., Hill B.J., Noto A., Ancuta P., Peretz Y., Fonseca S.G., Van Grevenynghe J., Boulassel M.R., Bruneau J., Shoukry N.H., Routy J.P., Douek D.C., Haddad E.K., Sekaly R.P. (2010). "Programmed death-1-induced interleukin-10 production by monocytes impairs CD4+ T cell activation during HIV infection". Natural Medicine 16 (4): 452–459. Tsuji M, Komatsu N, Kawamoto S, Suzuki K, Kanagawa O, Honjo T, Hori S, Fagarasan S. (2009). Preferential generation of follicular B helper T cells from Foxp3+ T cells in gut Peyer’s patches. Science. 323:1488–92. Wan, Y. Y & Flavell, R. A. (2007). Regulatory T-cell functions are subverted and converted owing to attenuated Foxp3 expression. Nature. 2007;445:766–70 Zhou X, Bailey-Bucktrout SL, Jeker LT, et al. (2009). Instability of the transcription factor Foxp3 leads to the generation of pathogenic memory T cells in vivo. Nat Immunol. 10:1000–7. Joetham A, Matsubara S, Okamoto M, Takeda K, Miyahara N, Dakhama A, Gelfand E. W. (2008). Plasticity of regulatory T cells: subversion of suppressive function and conversion to enhancement of lung allergic responses. J Immunol. 180:7117–24. Read More
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