期刊
JOURNAL OF IMMUNOLOGY
卷 198, 期 2, 页码 617-622出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1601762
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资金
- American Heart Association [16PRE27660002]
- National Institutes of Health/National Institute of Allergy and Infectious Diseases [T32AI007633, R01AI125446, R01AI127481]
- National Institutes of Health/National Institute of General Medical Sciences [8P20GM103447]
IL-10 is a pleiotropic cytokine expressed during malaria, a disease characterized by short-lived, parasite-specific Ab responses. The role of IL-10 in regulating B cell responses during malaria is not known. In this study we report that IL-10 is essential for anti-Plasmodium humoral immunity. We identify that germinal center (GC) B cell reactions, isotype-switched Ab responses, parasite control, and host survival require B cell-intrinsic IL-10 signaling. IL-10 also indirectly supports humoral immunity by suppressing excessive IFN-gamma, which induces T-bet expression in B cells. Genetic ablation of either IFN-gamma signaling or T-bet expression in B cells substantially enhanced GC B cell responses and anti-Plasmodium Ab production. Together, our data show that B cell-intrinsic IL-10 enhances whereas B cell-intrinsic IFN-g and T-bet suppress GC B cell responses and anti-Plasmodium humoral immunity. These data identify critical immunoregulatory circuits in B cells that may be targeted to promote long-lived humoral immunity and resistance to malaria.
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