| First Author | Chen GY | Year | 2009 |
| Journal | Science | Volume | 323 |
| Issue | 5922 | Pages | 1722-5 |
| PubMed ID | 19264983 | Mgi Jnum | J:244884 |
| Mgi Id | MGI:5913663 | Doi | 10.1126/science.1168988 |
| Citation | Chen GY, et al. (2009) CD24 and Siglec-10 selectively repress tissue damage-induced immune responses. Science 323(5922):1722-5 |
| abstractText | 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. |
