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Antiviral Immunity
Protective humoral immunity against viral infections requires an effective type 1 immune response by germinal center (GC) T and B cells, a hallmark of which is expression of the transcription factor T-bet. Mendoza et al. examined the coordinated activity of distinct T-bet–expressing lymphocyte populations during influenza infection in mice. They demonstrated that localization of T-bet+ TH1 cells to the T cell–B cell boundary opposite T-bet+ B cells, mediated by chemokine receptor CXCR3, is required for GC B cell class switching to antiviral immunoglobulin G2c (IgG2c). Conversely, T-bet+ T follicular helper cells controlled the magnitude of the GC B cell response but were dispensable for IgG2c class switching. These results demonstrate that the activities of T-bet+ T and B cells are spatiotemporally coordinated to control distinct features of the humoral response to viral infection.

Sci. Immunol. 6 , eabi4710 (2021).