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CD24 and Siglec-10 selectively repress tissue damage-induced immune responses.


ABSTRACT: 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 kappaB (NF-kappaB) 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.

SUBMITTER: Chen GY 

PROVIDER: S-EPMC2765686 | biostudies-literature | 2009 Mar

REPOSITORIES: biostudies-literature

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CD24 and Siglec-10 selectively repress tissue damage-induced immune responses.

Chen Guo-Yun GY   Tang Jie J   Zheng Pan P   Liu Yang Y  

Science (New York, N.Y.) 20090305 5922


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; negativel  ...[more]

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