2009/03/06 by Guo‐Yun Chen, Jie Tang, Pan Zheng +1 · 5 citations
Biochemistry, Genetics and Molecular Biology · Immunology and Microbiology · #Advanced Glycation End Products research #Glycosylation and Glycoproteins Research #Immune Response and Inflammation
paper · pdf · doi:10.1126/science.1168988
openalex publication_date 2009/03/06 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/01
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.