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.

尽管B细胞发育需要表达B细胞抗原受体（BCR），但尚不清楚自身抗原的结合是否对大多数B细胞产生积极影响。在这里，我们表明体内发展过程中通过自身配体的BCR参与导致Nod样受体成员Nod1的上调，该成员识别肠道共生细菌的产物。在缺乏自身Thy-1配体的抗胸腺细胞/ Thy-1自反应性BCR敲入小鼠中，发生了免疫球蛋白轻链编辑，产生了Nod1上调的B细胞，包括具有自然自身反应性的滤泡和边缘区B细胞。增加Nod1的BCR编辑导致优先生存。在正常的成年小鼠中，大多数成熟的B细胞都富含Nod1上调的细胞，通过Nod1发出的信号促进了成熟B细胞的竞争性存活。这些发现证明了微生物产物通过上调Nod1促进成熟B细胞存活的作用，为大多数B细胞的发育提供了BCR参与的积极作用。