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Inflammasomes and autoimmunity

Journal

TRENDS IN MOLECULAR MEDICINE
Volume 17, Issue 2, Pages 57-64

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2010.11.001

Keywords

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Funding

  1. National Institute of Health [AR056296, AI088177]
  2. Centers of Excellence for Influenza Research and Surveillance (CEIRS)
  3. American Lebanese Syrian Associated Charities (ALSAC)
  4. Arthritis Research UK
  5. [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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