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

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Kang, S; Keener, AB; Jones, SZ; Benschop, RJ; Caro-Maldonado, A; Rathmell, JC; Clarke, SH; Matsushima, GK; Whitmire, JK; Vilen, BJ

Published Date

  • January 1, 2016

Published In

Volume / Issue

  • 196 / 1

Start / End Page

  • 196 - 206

PubMed ID

  • 26621863

Pubmed Central ID

  • 26621863

Electronic International Standard Serial Number (EISSN)

  • 1550-6606

Digital Object Identifier (DOI)

  • 10.4049/jimmunol.1402527

Language

  • eng

Conference Location

  • United States