Article

Class switch recombination and somatic hypermutation in early mouse B cells are mediated by B cell and Toll-like receptors.

Program in Immunology and Department of Pathology, Sackler School of Graduate Biomedical Sciences and Tufts University School of Medicine, Boston, MA 02111, USA.
Immunity (Impact Factor: 19.75). 08/2007; 27(1):64-75. DOI: 10.1016/j.immuni.2007.05.018
Source: PubMed

ABSTRACT Activation-induced cytidine deaminase (AID) is required for immunoglobulin (Ig) gene class switch recombination (CSR), somatic hypermutation (SHM), and somatic hyperconversion. In general, high AID expression is found in mature B cells that are responding to antigens. However, AID expression and SHM have also been detected in developing B cells from transgenic mice that have a limited Ig repertoire. Here we demonstrate that AID expression, ongoing CSR, and active SHM occur in developing B cells from wild-type mice. Further, our results suggest that somatic variants arising from developing B cells in the bone marrow further diversify in the spleen of unimmunized mice. AID expression in developing B cells is T cell independent but involves engagement of B cell receptors and Toll-like receptors. Early AID expression can increase the preimmune repertoire of developing B cells, may provide an innate population of IgG- and IgA-expressing cells, and could be involved in receptor editing of self-reactive immature B cells.

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