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Accumulating evidence shows that B cells play an important role in infectious diseases. In the present study, the immune regulatory role of mature B cells in host defense to Pneumocystis was evaluated. Pneumocystis infection resulted in a decrease in B cells in patients and mice, and the Pneumocystis burden in B cell-deficient mice also progressively increased from weeks 1 to 7 after infection. The clearance of Pneumocystis was delayed in B cell-activating factor receptor (BAFF-R)-deficient mice (BAFF-R<jats:sup>\u2212\/\u2212<\/jats:sup>mice), which had few B cells and Pneumocystis-specific IgG and IgM antibodies, compared with clearance in wild-type (WT) mice. There were fewer effector CD4<jats:sup>+<\/jats:sup>T cells and higher percentages of T helper (Th)1\/Th17 cells in BAFF-R<jats:sup>\u2212\/\u2212<\/jats:sup>mice than in WT mice. Adoptive transfer of naive B cells, mRNA sequencing, and IL-1\u03b2 neutralization experiments indicated that IL-1\u03b2 is a likely determinant of the IL-10-producing B cell-mediated suppression of Th1\/Th17-cell immune responses in BAFF-R<jats:sup>\u2212\/\u2212<\/jats:sup>PCP mice. 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