Removal of autoreactive T and B cells outside of the primary lymphoid organs
In immunology, peripheral tolerance is the second branch of immunological tolerance, after central tolerance. It takes place in the immune periphery (after T and B cells egress from primary lymphoid organs). Its main purpose is to ensure that self-reactive T and B cells which escaped central tolerance do not cause autoimmune disease.[1] Peripheral tolerance can also serve a purpose in preventing an immune response to harmless food antigens and allergens.[2]
Self reactive cells are subject to clonal deletion or clonal diversion. Both processes of peripheral tolerance control the presence and production of self reactive immune cells.[3] Deletion of self-reactive T cells in the thymus is only 60-70% efficient, and naive T cell repertoire contains a significant portion of low-avidity self-reactive T cells. These cells can trigger an autoimmune response, and there are several mechanisms of peripheral tolerance to prevent their activation.[4] Antigen-specific mechanisms of peripheral tolerance include persistent of T cell in quiescence, ignorance of antigen and direct inactivation of effector T cells by either clonal deletion, conversion to regulatory T cells (Tregs) or induction of anergy.[5][4] Tregs, which are also generated during thymic T cell development, further suppress the effector functions of conventional lymphocytes in the periphery.[6] Dendritic cells (DCs) participate in the negative selection of autoreactive T cells in the thymus, but they also mediate peripheral immune tolerance through several mechanisms.[7]
Dependence of a particular antigen on either central or peripheral tolerance is determined by its abundance in the organism.[8] B Cells have a lower probability that they will express cell surface markers to pose the threat of causing an autoimmune attack.[9] Peripheral tolerance of B cells is largely mediated by B cell dependence on T cell help. However, B cell peripheral tolerance is much less studied.
^Janeway, Charles (2001-01-01). Immunobiology Five. Garland Pub. ISBN 9780815336426.
^Soyer, O. U.; Akdis, M.; Ring, J.; Behrendt, H.; Crameri, R.; Lauener, R.; Akdis, C. A. (2013). "Mechanisms of peripheral tolerance to allergens". Allergy. 68 (2): 161–170. doi:10.1111/all.12085. ISSN 1398-9995. PMID 23253293. S2CID 24008758.
^Xing, Yan; Hogquist, Kristin A. (June 2012). "T-Cell Tolerance: Central and Peripheral". Cold Spring Harbor Perspectives in Biology. 4 (6): a006957. doi:10.1101/cshperspect.a006957. ISSN 1943-0264. PMC 3367546. PMID 22661634.
^ abCite error: The named reference :3 was invoked but never defined (see the help page).
^Mueller, Daniel L (2010). "Mechanisms maintaining peripheral tolerance". Nature Immunology. 11 (1): 21–27. doi:10.1038/ni.1817. PMID 20016506. S2CID 9612138.
^Cretney, Erika; Kallies, Axel; Nutt, Stephen L. (2013). "Differentiation and function of Foxp3+ effector regulatory T cells". Trends in Immunology. 34 (2): 74–80. doi:10.1016/j.it.2012.11.002. PMID 23219401.
^Hasegawa, Hitoshi; Matsumoto, Takuya (2018). "Mechanisms of Tolerance Induction by Dendritic Cells In Vivo". Frontiers in Immunology. 9: 350. doi:10.3389/fimmu.2018.00350. ISSN 1664-3224. PMC 5834484. PMID 29535726.
^Malhotra, Deepali; Linehan, Jonathan L; Dileepan, Thamotharampillai; Lee, You Jeong; Purtha, Whitney E; Lu, Jennifer V; Nelson, Ryan W; Fife, Brian T; Orr, Harry T; Anderson, Mark S; Hogquist, Kristin A; Jenkins, Marc K (2016). "Tolerance is established in polyclonal CD4+ T cells by distinct mechanisms, according to self-peptide expression patterns". Nature Immunology. 17 (2): 187–195. doi:10.1038/ni.3327. PMC 4718891. PMID 26726812.
^Getahun, Andrew (May 2022). "The role of inhibitory signaling in peripheral B cell tolerance". Immunological Reviews. 307 (1): 27–42. doi:10.1111/imr.13070. ISSN 0105-2896. PMC 8986582. PMID 35128676.
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demyelinating polyneuropathy (CIDP) is an acquired autoimmune disease of the peripheral nervous system characterized by progressive weakness and impaired sensory...
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