Pharmacological manipulation of AID

In order to have an efficient humoral immune response, activated B lymphocytes with weak B cell receptor affinity for cognate antigen must undergo secondary antibody diversification. They do this using the mechanisms of somatic hypermutation (SHM), to boost the affinity of their antigen recognition domain, and class switch recombination (CSR), to exchange their effector domain, which specifies function. SHM and CSR are initiated by the enzyme Activation induced deaminase (AID), which transforms DNA deoxycytidine into deoxyuridine at the immunoglobulin (Ig) genes. A proportion of these mutagenic lesions are processed into other point mutations or DNA breaks to underpin antibody diversification. The lack of functional AID causes Hyper-IgM