期刊
JOURNAL OF IMMUNOLOGY
卷 192, 期 8, 页码 3740-3752出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1302561
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资金
- Fonds National de la Recherche Scientifique [FRSM FNRS 3.4.600.06]
- Communaute Francaise de Belgique [08/13-015]
- Fonds Emile Defay (Belgium)
- Fonds Van Buuren (Belgium)
- Fonds de la Recherche Scientifique-Fonds National de la Recherche Scientifique (Belgium)
- Agence Nationale pour la Recherche [ANR 2007 MIME-103-02]
- Fondation pour la Recherche Medicale [DAL 2007 0822007]
- Fonds Europeen de Developpement Regional [1575-32168]
- Le Studium, Orleans
Brucella spp are intracellular bacteria that cause brucellosis, one of the most common zoonoses in the world. Given the serious medical consequences of this disease, a safe and effective human vaccine is urgently needed. Efforts to develop this vaccine have been hampered by our lack of understanding of what constitutes a protective memory response against Brucella. In this study, we characterize the cells and signaling pathways implicated in the generation of a protective immune memory response following priming by the injection of heat-killed or live Brucella melitensis 16M. Using a panel of gene-deficient mice, we demonstrated that during a secondary recall response, both the Brucella-specific humoral response and CD4(+) Th1 cells must act together to confer protective immunity in the spleen to B. melitensis infection. Humoral protective immunity is induced by the inoculation of both heat-killed and live bacteria, and its development does not require T cells, MyD88/IL-12p35 signaling pathways, or an activation-induced deaminase-mediated isotype switch. In striking contrast, the presence of memory IFN-gamma-producing CD4(+) Th1 cells requires the administration of live bacteria and functional MyD88/IL-12p35 pathways. In summary, our work identifies several immune markers closely associated with protective immune memory and could help to define a rational strategy to obtain an effective human vaccine against brucellosis.
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