Somatic hypermutation

Somatic hypermutation (or SHM) is a cellular mechanism by which the immune system adapts to the new foreign elements that confront it (e.g. microbes). A major component of the process of affinity maturation, SHM diversifies B cell receptors used to recognize foreign elements (antigens) and allows the immune system to adapt its response to new threats during the lifetime of an organism.[1] Somatic hypermutation involves a programmed process of mutation affecting the variable regions of immunoglobulin genes. Unlike germline mutation, SHM affects only an organism's individual immune cells, and the mutations are not transmitted to the organism's offspring.[2] Because this mechanism is merely selective and not precisely targeted, somatic hypermutation has been strongly implicated in the development of B-cell lymphomas[3] and many other cancers.[4][5]

  1. ^ Janeway, C.A.; Travers, P.; Walport, M.; Shlomchik, M.J. (2005). Immunobiology (6th ed.). Garland Science. ISBN 978-0-8153-4101-7.
  2. ^ Oprea, M. (1999) Antibody Repertoires and Pathogen Recognition: Archived 2008-09-06 at the Wayback Machine The Role of Germline Diversity and Somatic Hypermutation (Thesis) University of Leeds.
  3. ^ Odegard V.H.; Schatz D.G. (2006). "Targeting of somatic hypermutation". Nat. Rev. Immunol. 6 (8): 573–583. doi:10.1038/nri1896. PMID 16868548. S2CID 6477436.
  4. ^ Steele, E.J.; Lindley, R.A. (2010). "Somatic mutation patterns in non-lymphoid cancers resemble the strand biased somatic hypermutation spectra of antibody genes" (PDF). DNA Repair. 9 (6): 600–603. doi:10.1016/j.dnarep.2010.03.007. PMID 20418189.
  5. ^ Lindley, R.A.; Steele, E.J. (2013). "Critical analysis of strand-biased somatic mutation signatures in TP53 versus Ig genes, in genome -wide data and the etiology of cancer". ISRN Genomics. 2013 Article ID 921418: 18 pages.