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Mice infected with the L3 of the filarial nematode Brugia pahangi make a strong T(h)2 response characterized by elevated levels of antigen-specific IL-4, IL-5 and IL-10. Here we show that B cells from these animals are the major proliferating population in vitro with depletion of B cells or infection of muMT mice, resulting in reduced levels of antigen-specific proliferation. B cells also act as antigen-presenting cells (APC) to CD4(+) cells as demonstrated by the switch in cytokine profiles upon B cell depletion. The efficiency of B cells in antigen presentation is attenuated by IL-10 which down-regulates the expression of B7-1 and B7-2 on the surface of B cells both in vitro and in vivo. Thus, IL-10 may modulate CD4 responses in L3-infected mice by suppressing the expression of B7 ligands on B cells. In support of this hypothesis, blockade of the IL-10R in vivo results in increased proliferation of CD4(+) cells. We propose that B cells participate in a negative feedback loop: IL-10 elicited by infection with L3 and produced by B cells (and CD4(+) cells) down-regulates the expression of B7 molecules on the B cell surface, attenuating their efficiency as APC to CD4(+) T cells and restricting their expansion.

B cells play a regulatory role in mice infected with the L3 of Brugia pahangi