Fc Receptor–Mediated Antibody Regulation of T Cell Immunity against Intracellular Pathogens

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Abstract
Immunity to intracellular microbial pathogens, including Chlamydia species, is controlled primarily by cell-mediated effector mechanisms, yet, the absence of antibodies results in inefficient microbial clearance. We investigated the hypothesis that certain Fc receptor functions promote the rapid induction of elevated T helper type 1 (Th1) response, which effectively clears chlamydiae. FcR−/− mice exhibited a delayed and reduced frequency of Chlamydia-specific Th1 cells, compared to FcR+/+ mice. In vitro, antichlamydial antibodies increased the rate of Th1 activation by FcR+/+ but not FcR−/− antigen-presenting cells. FcR−/− dendritic cells and the T cell–associated IgG2A and IgA mediate enhanced Th1 activation by antibodies. Immunization with chlamydia-antibody complexes induced elevated and protective Th1 response. These results provide a mechanistic basis for requiring both T cell and humoral immune responses in protective immunity and vaccine evaluation. Findings offer a paradigm in host defense wherein different effector components function indirectly to maximize the principal effector mechanism

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