| First Author | Han JH | Year | 2007 |
| Journal | Immunity | Volume | 27 |
| Issue | 1 | Pages | 64-75 |
| PubMed ID | 17658280 | Mgi Jnum | J:123630 |
| Mgi Id | MGI:3718931 | Doi | 10.1016/j.immuni.2007.05.018 |
| Citation | Han JH, et al. (2007) Class switch recombination and somatic hypermutation in early mouse B Cells are mediated by B Cell and toll-like receptors. Immunity 27(1):64-75 |
| abstractText | 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. |
