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Ann N Y Acad Sci ; 1063: 161-6, 2005 Dec.
Article in English | MEDLINE | ID: mdl-16481508

ABSTRACT

The resolution of Q fever, a zoonosis caused by Coxiella burnetii, depends on efficient innate and adaptive immune responses. Such responses are influenced by Toll-like receptors (TLRs). TLR4 is involved only in part in immune responses against C. burnetii, suggesting a role for TLR2. We investigated C. burnetii infection in wild-type and TLR2(-/-) mice. C. burnetii organisms were similarly eliminated by wild-type and TLR2(-/-) mice. In contrast, the formation of granulomas, a marker for efficient cell-mediated immunity, was markedly impaired. These results show that TLR2 is required for inflammatory and immune response to C. burnetii, but is dispensable for bacterial clearance.


Subject(s)
Coxiella burnetii/immunology , Inflammation Mediators/physiology , Q Fever/immunology , Q Fever/pathology , Toll-Like Receptor 2/physiology , Animals , Female , Granuloma/immunology , Granuloma/microbiology , Inflammation/immunology , Inflammation/metabolism , Inflammation/pathology , Liver/immunology , Liver/microbiology , Liver/pathology , Mice , Mice, Inbred BALB C , Mice, Inbred C57BL , Mice, Knockout , Q Fever/microbiology , Spleen/immunology , Spleen/microbiology , Spleen/pathology , Toll-Like Receptor 2/deficiency , Toll-Like Receptor 2/genetics
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