B cell-derived IL-27 promotes control of persistent LCMV infection

Recent studies have identified a critical role for B cell-produced cytokines in regulating both humoral and cellular immunity. Here, we show that B cells are an essential source of interleukin-27 (IL-27) during persistent lymphocytic choriomeningitis virus (LCMV) clone 13 (Cl-13) infection. By using conditional knockout mouse models with specific IL-27p28 deletion in B cells, we observed that B cell-derived IL-27 promotes survival of virus-specific CD4 T cells and supports functions of T follicular helper (Tfh) cells. Mechanistically, B cell-derived IL-27 promotes CD4 T cell function, antibody class switch, and the ability to control persistent LCMV infection. Deletion of IL-27ra in T cells demonstrated that T cell-intrinsic IL-27R signaling is essential for viral control, optimal CD4 T cell responses, and antibody class switch during persistent LCMV infection. Collectively, our findings identify a cellular mechanism whereby B cell-derived IL-27 drives antiviral immunity and antibody responses through IL-27 signaling on T cells to promote control of LCMV Cl-13 infection.

Automated summary

Recent studies have shown that B cells play a critical role in regulating immune responses through the production of cytokines, particularly interleukin-27 (IL-27). B cell-derived IL-27 promotes the survival and function of virus-specific CD4 T cells, as well as supporting the functions of T follicular helper (Tfh) cells. IL-27 signaling on T cells is essential for controlling viral infection and promoting optimal CD4 T cell responses and antibody class switch during persistent LCMV infection.