Somatic Hypermutation of Antigen Receptor Genes: Evolution


Analysis of the pattern of immunoglobulin mutation across species has helped to reveal some of the molecular properties of this process. Strong evidence for the involvement of a cytosine deaminase and error‐prone deoxyribonucleic acid (DNA) polymerases on the DNA encoding the immunoglobulin variable regions confirms earlier predictions made from phylogenetic studies.

Keywords: immunoglobulin; hypermutation; evolution; adaptive immunity; activation‐induced deaminase (AID)

Figure 1.

B cells that are activated by antigen form germinal centres in peripheral lymphoid organs such as the spleen and the lymph nodes. There, they divide for 7–21 days and these dividing cells are known as centroblasts. Centroblasts are where somatic hypermutation occurs in V(D)J regions. Subsequently, B cells can differentiate into centrocytes and test their immunoglobulin receptor affinity to antigen in the context of antigen‐presenting cells known as follicular dendritic cells. B cells whose receptors have acquired beneficial mutations are selected and differentiate into memory B cells, while the rest – the great majority – undergo apoptosis.



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Diaz, Marilyn, and Verkoczy, Laurent K(Mar 2008) Somatic Hypermutation of Antigen Receptor Genes: Evolution. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0006121.pub2]