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Inflammasome Activation by Adenylate Cyclase Toxin Directs Th17 Responses and Protection against Bordetella pertussis
- 1.0348119 - MBU-M 2011 RIV US eng J - Journal Article
Dunne, A. - Ross, P. J. - Pospíšilová, Eva - Mašín, Jiří - Meaney, A. - Sutton, C. E. - Iwakura, Y. - Tschopp, J. - Šebo, Peter - Mills, K. H. G.
Inflammasome Activation by Adenylate Cyclase Toxin Directs Th17 Responses and Protection against Bordetella pertussis.
Journal of Immunology. Roč. 187, č. 3 (2010), s. 1711-1719. ISSN 0022-1767
R&D Projects: GA ČR GA310/08/0447; GA AV ČR IAA500200914
Institutional research plan: CEZ:AV0Z50200510
Keywords : ADAPTIVE IMMUNE-RESPONSES * IL-17-PRODUCING T-CELLS * HOST-DEFENSE
Subject RIV: EC - Immunology
Impact factor: 5.745, year: 2010
In this article, we demonstrate that inflammasome-mediated IL-1b plays a critical role in promoting Ag-specific Th17 cells and in generating protective immunity against Bordetella pertussis infection. Using a murine respiratory challenge model, we demonstrated that the course of B. pertussis infection was significantly exacerbated in IL-1R type I-defective (IL-1RI2/2) mice. We found that adenylate cyclase toxin (CyaA), a key virulence factor secreted by B. pertussis, induced robust IL-1b production by dendritic cells through activation of caspase-1 and the NALP3-containing inflammasome complex. Using mutant toxins, we demonstrate that CyaA-mediated activation of caspase-1 was not dependent on adenylate cyclase enzyme activity but was dependent on the pore-forming capacity of CyaA
Permanent Link: http://hdl.handle.net/11104/0188731