Cited by 790Immune Response and InflammationInflammation biomarkers and pathwaysBiomarkers in Disease Mechanisms

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CD24 and Siglec-10 Selectively Repress Tissue Damage–Induced Immune Responses

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Chen, Guo-Yun, Tang, Jie, Zheng, Pan, Liu, Yang·2009·Science

DOI 10.1126/science.1168988PMC PMC2765686

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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.

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“The 76 aa CD24 mouse homologue interacts with Siglec-G to inhibit the macrophage response to damage-associated molecular patterns (DAMPs) [78].”
Excessive MYC Orchestrates Macrophages induced Chromatin Remodeling to Sustain Micropapillary‐Patterned Malignancy in Lung Adenocarcinoma
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“Although recent studies have greatly enhanced our understanding of the CD24/Siglec 10 pathway, there are still several challenging questions that remain to be answered.”
Background
Sialic Acid-Binding Ig-Like Lectins (Siglecs)
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“In addition, a study reported that CD24 was dominantly bound to siglec-10/G on liver oval cells, revealing that CD24 protected the liver against acetaminophen-induced hepatoxicity through regulating the inflammation (15,16).”
Background
813 CD24Fc ameliorates immune-related adverse events while preserving anti-tumor therapeutic effect
Liu, M., Wang, X., Zhang, P., Su, J., Du, X., Zhang, Y., Liu, Y., & Zheng, P. (2021) · Regular and Young Investigator Award Abstracts · doi:10.1136/jitc-2021-sitc2021.813 · Cited by 2
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CD24a knockout transforms the tumor microenvironment from cold to hot by promoting tumor-killing immune cell infiltration in a murine triple-negative breast cancer modelPreprint
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Kuralesova, A. I., Grosheva, A. G., Genkina, E. N., & Esmagambetov, I. B. (2025) · Biological Products Prevention Diagnosis Treatment · doi:10.30895/2221-996x-2025-25-3-343-356 · Cited by 1
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Self-citation
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“…patterns (PAMPs) and damage-associated molecular patterns (DAMPs), and C-type lectin domain family 4 member E ( CLEC4E /Mincle, FC = 5.75), a strong anti-inflammatory signal that promotes differentiation of T helper 2 (Th2) cells and suppression of inflammatory T helper 1 (Th1) cells [35–37].”
Influential
Realizing the potential of agonistic antibody immunotherapy
Cragg, M. S., Yu, X., Paluch, C., & Davis, S. J. (2026) · Nature Reviews Drug Discovery · doi:10.1038/s41573-026-01442-2 · Cited by 1
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Macrophage-directed therapeutic strategies in cancer
Joshi, S., & Varner, J. A. (2026) · Trends in cancer · doi:10.1016/j.trecan.2026.08.006 · Cited by 1
The CNS Innate Immune System and the Emerging Roles of the Neuroimmune Regulators (NIRegs) in Response to Infection, Neoplasia and Neurodegeneration
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Background
Linking Toll-Like Receptors Signaling to Oxidative Damage: Potential Role in Cancer Therapy
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Authors: Chen, G.-Y., Tang, J., Zheng, P., & Liu, Y.
Affiliations: Chinese Academy of Sciences (CN)
Corresponding author: Zheng, Pan
Liu, Yang
ORCID: Chen, Guo-Yun
Zheng, Pan
Liu, Yang
Venue: Science
Publisher: American Association for the Advancement of Science (AAAS)
Published: 2009-03-27
Volume: 323
Issue: 5922
Pages: 1722-1725
ISSN: 0036-8075 (ISSN-L)
1095-9203
DOI: 10.1126/science.1168988
PMC: PMC2765686
OpenAlex: W2158924104
Cited by: 786
References: 29
Citations by year: 2026: 36 · 2025: 51 · 2024: 43 · 2023: 46 · 2022: 55 · 2021: 64 · 2020: 45 · 2019: 23 · 2018: 28 · 2017: 34 · 2016: 47 · 2015: 44 · 2014: 53 · 2013: 58 · 2012: 37
FWCI: 22.46
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Science (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (5r01ai064350-15)
National Cancer Institute (R01CA112001, CA-58033, R01CA058033, CA112001)
National Institute of Allergy and Infectious Diseases (R01-AI064350, AI064350)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
Life Sciences › Immunology and Microbiology › Immunology › Biomarkers in Disease Mechanisms
Keywords: CD24, Siglec-10, Siglec-G, pattern recognition receptors, damage-associated molecular patterns, pathogen-associated molecular patterns, innate immune regulation, high mobility group box 1, HSP70, HSP90, NF-κB activation, tissue damage
MeSH terms: Acetaminophen, Animals, Dendritic Cells, Humans, Immunity, Innate, Inflammation, Lipopolysaccharides, Liver, Necrosis, Receptors, Antigen, B-Cell, Receptors, Cell Surface, Signal Transduction, Cytokines, Protein Structure, Tertiary, HSP70 Heat-Shock Proteins, HSP90 Heat-Shock Proteins, HMGB1 Protein, Lectins, Immunoprecipitation, Mutant Proteins, Receptors, Pattern Recognition, Mice, CD24 Antigen, Transcription Factor RelA, Protein Tyrosine Phosphatase, Non-Receptor Type 6, Sialic Acid Binding Immunoglobulin-like Lectins

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CD24 and Siglec-10 Selectively Repress Tissue Damage–Induced Immune Responses

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