Nitric oxide controls the immunopathology of tuberculosis by inhibiting NLRP3 inflammasome–dependent processing of IL-1β

Chronic infections can result in harmful production of the proinflammatory cytokine IL-1 generated via the NLRP3 inflammasome. Sassetti et al . demonstrate that IL-1 activated by Mycobacteria results in nitrosylation and consequent regulation of the NLRP3 inflammasome. Interleukin 1 (IL-1) is an imp...

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Veröffentlicht in:	Nature immunology 2013-01, Vol.14 (1), p.52-60
Hauptverfasser:	Mishra, Bibhuti B, Rathinam, Vijay A K, Martens, Gregory W, Martinot, Amanda J, Kornfeld, Hardy, Fitzgerald, Katherine A, Sassetti, Christopher M
Format:	Artikel
Sprache:	eng
Schlagworte:	631/250/255/1856 631/250/256/2177 631/250/516 Animals Antimicrobial agents Biomedicine Carrier Proteins - genetics Carrier Proteins - metabolism Cells, Cultured Control Genetic aspects Health aspects Humans Immunity, Innate Immunology Infectious Diseases Inflammasomes - metabolism Interferon-gamma - genetics Interleukin-1beta - metabolism Interleukins Mice Mice, Inbred C57BL Mice, Knockout Mycobacterium tuberculosis Mycobacterium tuberculosis - immunology Nitric oxide Nitric Oxide - immunology Nitric Oxide - metabolism NLR Family, Pyrin Domain-Containing 3 Protein Protein Modification, Translational - genetics Protein Modification, Translational - immunology Protein Multimerization - genetics Protein Multimerization - immunology Risk factors Signal Transduction - genetics Signal Transduction - immunology Tuberculosis Tuberculosis - immunology
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