NLR Nod1 signaling promotes survival of BCR-engaged mature B cells through up-regulated Nod1 as a positive outcome

Kyoko Hayakawa, Anthony M. Formica, Yan Zhou, Daiju Ichikawa, Masanao Asano, Yue Sheng Li, Susan A. Shinton, Joni Brill-Dashoff, Gabriel Núñez, Richard R. Hardy

研究成果: Article査読

8 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)3067-3083
ページ数17
ジャーナルJournal of Experimental Medicine
214
10
DOI
出版ステータスPublished - 2017

ASJC Scopus subject areas

  • 医学(全般)

フィンガープリント

「NLR Nod1 signaling promotes survival of BCR-engaged mature B cells through up-regulated Nod1 as a positive outcome」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル