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.

RGYW (i.e. A/G G C/T A/T) for a G, WRCY for a C, WA for an A and TW for a T.[7][8] The overall result of the hypermutation process is achieved by a balance between error-prone and high fidelity repair.

[9] This directed hypermutation allows for the selection of B cells that express immunoglobulin receptors possessing an enhanced ability to recognize and bind a specific foreign antigen.

This kind of gene conversion is also started by the AID enzyme, leading to a double-strand break, which is then repaired by using other V or pseudogenic-V segments as templates.

Simplistic overview of V(D)J recombination and somatic hypermutations at the immunoglobulin heavy chain variable region. Abbreviation of the regions: C = constant, D = diversity, J = joining, V = variable, L = light, H = heavy, FW = frame work, CDR = complementarity-determining regions, N = junctional diversity sequence.
Cytosine
Uracil