Title: IgG-Immune Complexes Promote B Cell Memory by Inducing BAFF.

Authors: Kang, SunAh; Keener, Amanda B; Jones, Shannon Z; Benschop, Robert J; Caro-Maldonado, Alfredo; Rathmell, Jeffrey C; Clarke, Stephen H; Matsushima, Glenn K; Whitmire, Jason K; Vilen, Barbara J

Published In J Immunol, (2016 Jan 01)

Abstract: Memory B cell responses are vital for protection against infections but must also be regulated to prevent autoimmunity. Cognate T cell help, somatic hypermutation, and affinity maturation within germinal centers (GCs) are required for high-affinity memory B cell formation; however, the signals that commit GC B cells to the memory pool remain unclear. In this study, we identify a role for IgG-immune complexes (ICs), FcγRs, and BAFF during the formation of memory B cells in mice. We found that early secretion of IgG in response to immunization with a T-dependent Ag leads to IC-FcγR interactions that induce dendritic cells to secrete BAFF, which acts at or upstream of Bcl-6 in activated B cells. Loss of CD16, hematopoietic cell-derived BAFF, or blocking IC:FcγR regions in vivo diminished the expression of Bcl-6, the frequency of GC and memory B cells, and secondary Ab responses. BAFF also contributed to the maintenance and/or expansion of the follicular helper T cell population, although it was dispensable for their formation. Thus, early Ab responses contribute to the optimal formation of B cell memory through IgG-ICs and BAFF. Our work defines a new role for FcγRs in GC and memory B cell responses.

PubMed ID: 26621863

MeSH Terms: No MeSH terms associated with this publication