Journal
TRENDS IN MOLECULAR MEDICINE
Volume 17, Issue 2, Pages 57-64Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2010.11.001
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Funding
- National Institute of Health [AR056296, AI088177]
- Centers of Excellence for Influenza Research and Surveillance (CEIRS)
- American Lebanese Syrian Associated Charities (ALSAC)
- Arthritis Research UK
- [FP7-HEALTH-2007-2.4.4-1]
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The NOD-like receptor (NLR) family members are cytosolic sensors of microbial components and danger signals. A subset of NLRs control inflammasome assembly that results in caspase-1 activation and, in turn, IL-1 beta and IL-18 production. Excessive inflammasome activation can cause autoinflammatory disorders, including the hereditary periodic fevers. Autoinflammatory and autoimmune diseases form a disease spectrum of aberrant, immune-mediated inflammation against self, through innate and adaptive immunity. However, the role of inflammasomes in autoimmune disease is less clear than in autoinflammation, despite the numerous effects IL-1 beta and IL-18 can have on shaping adaptive immunity. We summarize the role of inflammasomes in autoimmune disorders, highlight the need for a better understanding of inflammasomes in these conditions and offer suggestions for future research directions.
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