Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 119, Issue 3, Pages -Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.2116741119
Keywords
IL-27; viral infection; B cells; CD4 T cells; antibody
Categories
Funding
- NIH [R01AI164744, R01AI118862]
- Cancer Research Institute/Irvington postdoctoral fellowship
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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.
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.
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