期刊
TRENDS IN IMMUNOLOGY
卷 31, 期 5, 页码 171-175出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.it.2010.01.007
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资金
- Institut Pasteur de Lille
- INSERM
- Region Nord Pas de Calais
- Fondation pour la Recherche Medicale
- Bill and Melinda Gates Foundation
- Foundation for the National Institutes of Health
- Canadian Institutes for Health Research through the Grand Challenges in Global Health Initiative
- University of British Columbia
Candida albicans is a diploid fungus that colonizes the gastrointestinal tract asymptomatically in a large proportion of the human population, but can cause life-threatening conditions in immunocompromised patients. Recent immunological investigations have revealed the Nod-like receptor pyrin domain-containing protein 3 (NLRP3) to be a cytosolic surveillance mechanism against germinating Candida. These observations point to the idea of a molecular link between Candida and a spectrum of auto-inflammatory diseases. When excessive activation of NLRP3 occurs, it can confer resistance against disseminating Candida infection but might also cause NLRP3-associated periodic syndromes. Alternatively, we propose a pathophysiological model whereby a defective NLRP3-coupled inflammasome can result in enhanced mucosal colonization of granuloma-provoking microorganisms, including C. albicans, precipitating the formation of Crohn's disease-associated inflammatory lesions.
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