FcγRIIb and BAFF differentially regulate peritoneal B1 cell survival

AMEZCUA VESELY, MARIA CAROLINA; SCHWARTZ, MARC; BERMEJO, DANIELA A.; MONTES, CAROLINA L.; CAUTIVO, KELLY M.; KALERGIS, ALEXIS M.; RAWLINGS, DAVID J.; ACOSTA-RODRÍGUEZ, EVA V.; GRUPPI, ADRIANA

JOURNAL OF IMMUNOLOGY

AMER ASSOC IMMUNOLOGISTS

Año: 2012 vol. 188 p. 4792 - 4792

0022-1767

1 cells produce most natural Abs in unimmunized mice and play a key role in the response to thymus-independent Ags and microbial infection. Enlargement of B1 cell number in mice is often associated with autoimmunity. However, the factors that control peripheral B1 cell survival remain poorly characterized. Mice lacking the inhibitory receptor FcγRIIb exhibit a massive expansion in peritoneal B1 cells, implicating this receptor in B1 cell homeostasis. In this study, we show that peritoneal B1 cells express the highest levels of FcγRIIb among B cell subsets and are highly susceptible to FcγRIIb-mediated apoptosis. B1 cells upregulate FcγRIIb in response to innate signals, including CpG, and the B cell homeostatic cytokine BAFF efficiently protects activated B1 cells from FcγRIIb-mediated apoptosis via receptor downregulation. BAFF-transgenic mice manifest an expansion of peritoneal B1 cells that express lower levels of FcγRIIb and exhibit reduced susceptibi