HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

Published online before print November 2, 2007

This Article Full Text Full Text (PDF) All Versions of this Article: jlb.0607362v1 83/3/507    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Martinon, F. PubMed PubMed Citation Articles by Martinon, F.

(Journal of Leukocyte Biology. 2008;83:507-511.)
© 2008 by Society for Leukocyte Biology

Detection of immune danger signals by NALP3

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

¹Correspondence: Dept. of Immunology and Infectious Diseases, Harvard School of Public Health, 651 Huntington Ave., Boston, MA 02115, USA. 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