| First Author | Salek-Ardakani S | Year | 2011 |
| Journal | J Immunol | Volume | 186 |
| Issue | 9 | Pages | 5294-303 |
| PubMed ID | 21441451 | Mgi Jnum | J:172856 |
| Mgi Id | MGI:5009147 | Doi | 10.4049/jimmunol.1100406 |
| Citation | Salek-Ardakani S, et al. (2011) B cell-specific expression of B7-2 is required for follicular Th cell function in response to vaccinia virus. J Immunol 186(9):5294-303 |
| abstractText | Follicular Th (T(FH)) cells are specialized in provision of help to B cells that is essential for promoting protective Ab responses. CD28/B7 (B7-1 and B7-2) interactions are required for germinal center (GC) formation, but it is not clear if they simply support activation of naive CD4 T cells during initiation of responses by dendritic cells or if they directly control T(FH) cells and/or directly influence follicular B cell differentiation. Using a model of vaccinia virus infection, we show that B7-2 but not B7-1 deficiency profoundly impaired T(FH) cell development but did not affect CD4 T cell priming and Th1 differentiation. Consistent with this, B7-2 but not B7-1 was required for acquisition of GC B cell phenotype, plasma cell generation, and virus-specific neutralizing Ab responses. Mixed adoptive transfer experiments indicated that bidirectional interactions between CD28 expressed on activated T cells and B7-2 expressed on follicular B cells were essential for maintenance of the T(FH) phenotype and GC B cell development. Our data provide new insight into the source and nature of molecules required for T(FH) cells to direct GC B cell responses. |
