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Helper T-cells (TH or Th cells) are a subtype of CD4+ T-cells that cooperate with other lymphocytes (e.g., B-cells or cytotoxic T-cells) to initiate a number of immune responses.[1] They are the major variety of T-cell affected by HIV infection.[2] Naïve TH cells are initially exposed to an antigen (via antigen-presenting cells, such as dendritic cells or macrophages), then they proliferate and their daughter cells differentiate into several effector TH cells, which are generally classified based on their cytokine secretion patterns, along with their function and the cytokines that induce them (that is, the cytokines that stimulate their formation if present at the time of antigen-presentation). Major effector TH cells include: TH1 cells, TH2 cells and TH17 cells.[3]

TH1 cells are helper T-cells primed to promote defences against intracellular microbes (e.g., Mycobacterium tuberculosis), the major cytokines they produce include IFN-γ, IL-2, IL-18 and TNF-β.[4][5] Whereas cytokines that induce this particular subset of helper cells include: IFN-γ and IL-12.[3] They activate macrophages (via their release of IFN-γ) and in doing so potentiate their microbicidal effects against pathogens, especially intracellular pathogens. They also promote the production of IgG antibodies by activated B-cells. They play a crucial role in some autoimmune/chronic inflammatory diseases, especially those characterized by the formation of granulomas such as Crohn disease and sarcoidosis.

TH2 cells are helper cells that are designed to defend the body against larger pathogens, especially helminths (worms). They secrete interleukin-4, interleukin-5 and interleukin-13: interleukin-4 stimulates the proliferation of mast cells, B-cells and T-cells (and also promotes the formation of TH2 cells in the first place) along with class switching of antigen-activated B-cells to IgE production. Interleukin-5 stimulates the activation and differentiation of eosinophils and stimulates antigen-induced differentiation of B-cells into plasma cells. Interleukin-13 enhances IgE production by B-cells and stimulates mucus secretion.[3]

TH17 cells are specifically designed to stimulate phagocytes like neutrophils and monocytes (e.g., macrophages) to engulf and digest extracellular bacteria and pathogenic fungi. It plays a crucial role in the pathophysiology of inflammatory bowel disease, multiple sclerosis and psoriasis.[3]

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Reference listEdit

  1. Kilbourne, J; Case, JT; Cho, DS; Hui, C; Jarnot, M; Koroma, B; Pash, J; Powell, T; Schulman, JL; Sorden, N (2015). "T-Lymphocytes, Helper-Inducer". Medical Subject Headings. Bethesda, USA: U.S. National Library of Medicine. Retrieved 21 December 2014. 
  2. Kumar, V; Abbas, AK; Aster, AC (July 2014). "Chapter 6. Diseases of the Immune System". Robbins & Cotran Pathologic Basis of Disease 9e. Philadelphia, USA: Saunders. p. 245. ISBN 978-0-8089-2450-0. 
  3. 3.0 3.1 3.2 3.3 Kumar, V; Abbas, AK; Aster, AC (July 2014). "Chapter 6. Diseases of the Immune System". Robbins & Cotran Pathologic Basis of Disease 9e. Philadelphia, USA: Saunders. pp. 197–198. ISBN 978-0-8089-2450-0. 
  4. Mosmann, TR; Kobie, JJ; Lee, FE; Quataert, SA (December 2009). "T helper cytokine patterns: defined subsets, random expression, and external modulation.". Immunologic Research 45 (2-3): 173–84. PMID 19198763. doi:10.1007/s12026-009-8098-5. 
  5. Novick, D; Kim, S; Kaplanski, G; Dinarello, CA (15 December 2013). "Interleukin-18, more than a Th1 cytokine.". Seminars in Immunology 25 (6): 439–48. PMID 24275602. doi:10.1016/j.smim.2013.10.014. 

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