| First Author | Kang S | Year | 2016 |
| Journal | J Immunol | Volume | 196 |
| Issue | 1 | Pages | 196-206 |
| PubMed ID | 26621863 | Mgi Jnum | J:244913 |
| Mgi Id | MGI:5913692 | Doi | 10.4049/jimmunol.1402527 |
| Citation | Kang S, et al. (2016) IgG-Immune Complexes Promote B Cell Memory by Inducing BAFF. J Immunol 196(1):196-206 |
| abstractText | 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), FcgammaRs, 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-FcgammaR 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:FcgammaR 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 FcgammaRs in GC and memory B cell responses. |
