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J Infect Dis ; 188(4): 617-24, 2003 Aug 15.
Article in English | MEDLINE | ID: mdl-12898452

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.


Subject(s)
Chlamydia Infections/immunology , Receptors, Fc/immunology , Th1 Cells/immunology , Animals , Antibodies, Bacterial/immunology , Antigens, Bacterial/immunology , Chlamydia/immunology , Dendritic Cells/immunology , Female , Gene Deletion , Genitalia, Female/immunology , Genitalia, Female/microbiology , Lymphocyte Activation/immunology , Mice , Mice, Knockout , Mucous Membrane/immunology , Mucous Membrane/microbiology , Receptors, Fc/genetics
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