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Published online before print November 2, 2007

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0607362

Received for publication June 8, 2007.
Revised September 13, 2007.
Accepted for publication October 4, 2007.

Article

Detection of immune danger signals by NALP3

Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, USA

^@ To whom correspondence should be addressed. E-mail: fmartino{at}hsph.harvard.edu.

	Abstract

The innate immune system in animals has been forged to detect microbes, coordinate symbiotic responses, and mount immune defenses against pathogens. Recently, innate immunity was shown to detect signals released by damaged cells or tissues such as uric acid or ATP. These danger signals were proposed to be important in promoting and regulating inflammation upon trauma or pathogen insults. The physiological relevance of these signals in the immune response and their mechanisms of action are still unclear. Recent findings suggest that some danger signals activate the NALP3 inflammasome, an innate immune complex that controls inflammatory caspases and IL-1 activation.

Key Words: inflammasome • autoinflammation • uric acid • gout