Journal
JOURNAL OF IMMUNOLOGY
Volume 186, Issue 9, Pages 5294-5303Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1100406
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Funding
- National Institutes of Health [AI77079, CA91837, AI67341, AI63107, AI72543]
- Center for Infectious Disease at the La Jolla Institute for Allergy and Immunology
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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. The Journal of Immunology, 2011, 186: 5294-5303.
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