NLRC4 inflammasomes in dendritic cells regulate noncognate effector function by memory CD8(+) T cells.
SourceNature Immunology, 13, 2, (2012), pp. 162-9
01 februari 2012
Article / Letter to editor
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Paediatrics - OUD tm 2017
Laboratory of Genetic, Endocrine and Metabolic Diseases
SubjectIGMD 3: Genomic disorders and inherited multi-system disorders N4i 4: Auto-immunity, transplantation and immunotherapy; N4i 1: Pathogenesis and modulation of inflammation NCMLS 1: Infection and autoimmunity
Memory T cells exert antigen-independent effector functions, but how these responses are regulated is unclear. We discovered an in vivo link between flagellin-induced NLRC4 inflammasome activation in splenic dendritic cells (DCs) and host protective interferon-gamma (IFN-gamma) secretion by noncognate memory CD8(+) T cells, which could be activated by Salmonella enterica serovar Typhimurium, Yersinia pseudotuberculosis and Pseudomonas aeruginosa. We show that CD8alpha(+) DCs were particularly efficient at sensing bacterial flagellin through NLRC4 inflammasomes. Although this activation released interleukin 18 (IL-18) and IL-1beta, only IL-18 was required for IFN-gamma production by memory CD8(+) T cells. Conversely, only the release of IL-1beta, but not IL-18, depended on priming signals mediated by Toll-like receptors. These findings provide a comprehensive mechanistic framework for the regulation of noncognate memory T cell responses during bacterial immunity.
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