Journal
SCIENCE
Volume 323, Issue 5922, Pages 1722-1725Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1168988
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Funding
- NIH [AI064350, CA58033, CA112001]
- U.S. department of Defense [W81XWH-08-1-0036]
- Natural Science Foundation of China [30640420558]
- Ministry of Science and Technology of China [2006CB910901]
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Patten recognition receptors, which recognize pathogens or components of injured cells (danger), trigger activation of the innate immune system. Whether and how the host distinguishes between danger-versus pathogen-associated molecular patterns remains unresolved. We report that CD24-deficient mice exhibit increased susceptibility to danger- but not pathogen-associated molecular patterns. CD24 associates with high mobility group box 1, heat shock protein 70, and heat shock protein 90; negatively regulates their stimulatory activity; and inhibits nuclear factor kappa B (NF-kappa B) activation. This occurs at least in part through CD24 association with Siglec-10 in humans or Siglec-G in mice. Our results reveal that the CD24-Siglec G pathway protects the host against a lethal response to pathological cell death and discriminates danger-versus pathogen-associated molecular patterns.
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