| First Author | Hayakawa K | Year | 2017 |
| Journal | J Exp Med | Volume | 214 |
| Issue | 10 | Pages | 3067-3083 |
| PubMed ID | 28878001 | Mgi Jnum | J:253155 |
| Mgi Id | MGI:5924583 | Doi | 10.1084/jem.20170497 |
| Citation | Hayakawa K, et al. (2017) NLR Nod1 signaling promotes survival of BCR-engaged mature B cells through up-regulated Nod1 as a positive outcome. J Exp Med 214(10):3067-3083 |
| abstractText | Although B cell development requires expression of the B cell antigen receptor (BCR), it remains unclear whether engagement of self-antigen provides a positive impact for most B cells. Here, we show that BCR engagement by self-ligand during development in vivo results in up-regulation of the Nod-like receptor member Nod1, which recognizes the products of intestinal commensal bacteria. In anti-thymocyte/Thy-1 autoreactive BCR knock-in mice lacking self-Thy-1 ligand, immunoglobulin light chain editing occurred, generating B cells with up-regulated Nod1, including follicular and marginal zone B cells with natural autoreactivity. This BCR editing with increased Nod1 resulted in preferential survival. In normal adult mice, most mature B cells are enriched for Nod1 up-regulated cells, and signaling through Nod1 promotes competitive survival of mature B cells. These findings demonstrate a role for microbial products in promoting survival of mature B cells through up-regulated Nod1, providing a positive effect of BCR engagement on development of most B cells. |
