Reviews:
AIDinduced remodeling of immunoglobulin genes and B cell fate
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Brice Laffleur1,2, Nicolas Denis-Lagache1,2, Sophie Péron1,2, Christophe Sirac1,2, Jeanne Moreau1,2 and Michel Cogné1,2,3
1 Limoges University, Limoges France ;
2 Centre National de la Recherche Scientifique,
3 Institut Universitaire de France, Limoges, France
Correspondence:
Michel Cogné, email:
Keywords: AID; B cell fate; BCR, immunoglobulin genes
Received: October 28, 2013 Accepted: December 12, 2013 Published: December 14, 2013
Abstract
Survival and phenotype of normal and malignant B lymphocytes are critically dependent on constitutive signals by the B cell receptor (BCR) for antigen. In addition, either antigen ligation of the BCR or various mitogenic stimuli result in B cell activation and induction of activation-induced deaminase (AID). AID activity can in turn mediate somatic hypermutation (SHM) of immunoglobulin (Ig) V regions and also deeply remodel the Ig heavy chain locus through class switch recombination (CSR) or locus suicide recombination (LSR). In addition to changes linked to affinity for antigen, modifying the class/isotype (i.e. the structure and function) of the BCR or suddenly deleting BCR expression also modulates the fate of antigen-experienced B cells.