| First Author | Moore T | Year | 2003 |
| Journal | J Infect Dis | Volume | 188 |
| Issue | 4 | Pages | 617-24 |
| PubMed ID | 12898452 | Mgi Jnum | J:120672 |
| Mgi Id | MGI:3707637 | Doi | 10.1086/377134 |
| Citation | Moore T, et al. (2003) Fc receptor-mediated antibody regulation of T cell immunity against intracellular pathogens. J Infect Dis 188(4):617-24 |
| abstractText | 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. |
