CD24 and Siglec-10 Selectively Repress Tissue Damage–Induced Immune Responses
Open accessAbstract
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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Inhibitory Siglec recognition of cell surface sialoglycans is a clear example of glycan-based self-associated molecular patterns (SAMPs), which may provide a mechanism for the host to discriminate between infectious nonself and noninfectious self.
“A clear example of glycan-based SAMPs has been reported in the form of inhibitory Siglec recognition of cell surface sialoglycans (962 -964), which may also provide a mechanism for the host to discriminate between infectious nonself and noninfectious self (965).”
From Biological roles of glycans (2017) · cites this paper as [963]
CD24-mediated inhibition was associated with increased pro-inflammatory cytokine production by HMGB1 and decreased survival following acetaminophen-induced liver injury.
“CD24-mediated inhibition was associated with increased pro-inflammatory cytokine production by HMGb1 and decreased survival following acetaminophen-induced liver injury106.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [106]
CD24 can bind both HMGB1 and HSPs.
“Specifically, CD24, which can bind to both HMGb1 and HSPs, negatively regulates sterile inflammatory responses.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [106]
DAMP-specific receptors can negatively regulate inflammatory responses.
“It has also been shown that DAMP-specific receptors can negatively regulate inflammatory responses.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [106]
CD24 negatively regulates sterile inflammatory responses.
“Specifically, CD24, which can bind to both HMGb1 and HSPs, negatively regulates sterile inflammatory responses.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [106]
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“, 2010), and cluster of differentiation 24 (CD24)/Siglec-10 (Chen et al., 2009), thereby functioning as a DAMP that alerts, recruits, and activates innate immune cells to produce a wide range of cytokines and chemokines.”
BackgroundKuo, C. S., Pavlidis, S. P., Loza, M. J., Baribaud, F., Rowe, A., Pandis, I., Sousa, A. R., Corfield, J., Djukanović, R., Lutter, R., et al. (2017) · European Respiratory Journal · doi:10.1183/13993003.02135-2016 · Cited by 370 · see citing works
High Mobility Group Box Protein 1 (HMGB1): The Prototypical Endogenous Danger Molecule
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“CD24 also has the ability to interact with human Siglec-10 but not with Siglecs -7, -9 and -11 (83, 84).”
BackgroundApoptosis and Necrosis in the Liver
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“Initially, apart from various pathogens, membrane-damaged necrotic cells were also found to directly stimulate an immunogenic response (e.g., by promoting a cytotoxic T-cell response and inducing DC activation) in the absence of exogenous adjuvants.107,108 Importantly, the immunostimulatory activity of membrane-damage…”
BackgroundInfluentialDAMPs, MAMPs, and NAMPs in plant innate immunity
Choi, H. W., & Klessig, D. F. (2016) · BMC Plant Biology · doi:10.1186/s12870-016-0921-2 · Cited by 356 · see citing works
“Siglec-10 k CD24 [72]”
Regulatory Circuits Mediated by Lectin-Glycan Interactions in Autoimmunity and Cancer
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High-mobility group box 1 protein (HMGB1) operates as an alarmin outside as well as inside cells
Andersson, U., Yang, H., & Harris, H. (2018) · Seminars in Immunology · doi:10.1016/j.smim.2018.02.011 · Cited by 309 · see citing works
HMGB1 as a therapeutic target in disease
Xue, J., Suarez, J. S., Minaai, M., Li, S., Gaudino, G., Pass, H. I., Carbone, M., & Yang, H. (2020) · Journal of Cellular Physiology · doi:10.1002/jcp.30125 · Cited by 297 · see citing works
“HMGB1, Siglec‐10, and CD24 seem to form a trimer and regulate acetaminophen‐induced inflammation through the NF‐κB pathway (G. Y. Chen et al., 2009).”
BackgroundRosin, D. L., & Okusa, M. D. (2011) · Journal of the American Society of Nephrology · doi:10.1681/asn.2010040430 · Cited by 284 · see citing works
Emerging phagocytosis checkpoints in cancer immunotherapy
Liu, Y., Wang, Y., Yang, Y., Weng, L., Wu, Q., Zhang, J., Zhao, P., Fang, L., Shi, Y., & Wang, P. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01365-z · Cited by 287 · see citing works
Self-citationXu, G., Jin, J., Fu, Z., Wang, G., Lei, X., Xu, J., & Wang, J. (2025) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-025-02312-w · Cited by 309 · see citing works
“Representative results were obtained from a series of studies on CD24, which binds to damage-associated molecular patterns to inhibit in fl ammatory responses mediated by NF-κ B pathway activation 101,102 .”
Chen, W., Han, C., Xie, B., Hu, X., Yu, Q., Shi, L., Wang, Q., Li, D., Wang, J., Zheng, P., et al. (2013) · Cell · doi:10.1016/j.cell.2013.01.011 · Cited by 274 · see citing works
“Although CD24 and some sialic acids are known as ligands for Siglec-G (Chen et al., 2009), we confirmed that negative function of Siglec-G in VSV-induced IFN-b production is not dependent on its interaction with CD24 molecule or other sialic acids presented on the cell surface of macrophages.”
BackgroundInfluentialSelf-citationFang, X., Zheng, P., Tang, J., & Liu, Y. (2010) · Cellular and Molecular Immunology · doi:10.1038/cmi.2009.119 · Cited by 274 · see citing works
Self-citationMicroglia in ischemic brain injury
Weinstein, J. R., Koerner, I. P., & Möller, T. (2009) · Future Neurology · doi:10.2217/fnl.10.1 · Cited by 268 · see citing works
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Varki, A. (2011) · Glycobiology · doi:10.1093/glycob/cwr087 · Cited by 263 · see citing works
“, “CD24 is the ligand for Siglec-G/ 10” (Chen et al. 2009), such specific cognate glycoform ligands might best designated by a superscript (Varki 2009).”
BackgroundPhysiological Signaling Functions of Reactive Oxygen Species in Stem Cells: From Flies to Man
Sinenko, S. A., Starkova, T. Y., Kuzmin, A. A., & Tomilin, A. N. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.714370 · Cited by 256 · see citing works
The danger theory: 20 years later
Pradeu, T., & Cooper, E. L. (2012) · Frontiers in Immunology · doi:10.3389/fimmu.2012.00287 · Cited by 251 · see citing works
“Thus, even though HSPs have been considered as the paradigmatic example of DAMPs, no consensus has yet been reached on this claim.”
BackgroundInfluentialTamai, K., Yamazaki, T., Chino, T., Ishii, M., Otsuru, S., Kikuchi, Y., Iinuma, S., Saga, K., Nimura, K., Shimbo, T., et al. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1016753108 · Cited by 244 · see citing works
“Indeed, freeHMGB1, that is unbound to endogenous/exogenous inflammatory factors, is able to suppress inflammatory reactions in noninjured tissues by inhibiting TLRmediated NF-κB signaling (33).”
BackgroundHMGB1 as biomarker and drug target
Vénéreau, E., Leo, F. D., Mezzapelle, R., Careccia, G., Musco, G., & Bianchi, M. E. (2016) · Pharmacological Research · doi:10.1016/j.phrs.2016.06.031 · Cited by 240 · see citing works
Infections and autoimmunity: the multifaceted relationship
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“[52] demonstrated that CD24 associates with DAMPs and through interaction with sialic acid-binding Ig-like lectin-10, negatively regulates their stimulatory activity and inhibits NF- B activation.”
BackgroundThe Spectrum of Achalasia: Lessons From Studies of Pathophysiology and High-Resolution Manometry
Kahrilas, P. J., & Boeckxstaens, G. E. (2013) · Gastroenterology · doi:10.1053/j.gastro.2013.08.038 · Cited by 234 · see citing works
Martin-Murphy, B. V., Holt, M. R., & Ju, C. (2009) · Toxicology Letters · doi:10.1016/j.toxlet.2009.11.016 · Cited by 226 · see citing works
“A more recent publication provides insight into the mechanism of HMGB1-induced inflammation (Chen et al., 2009).”
BackgroundInnate and adaptive immune responses to cell death
Rock, K. L., Lai, J., & Kono, H. (2011) · Immunological Reviews · doi:10.1111/j.1600-065x.2011.01040.x · Cited by 220 · see citing works
“CD24, Siglec-10 ⁄ G), which then serve to limit the magnitude of the inflammatory responses (102).”
BackgroundWilk, A. J., Lee, M. J., Wei, B., Parks, B. E., Pi, R., Martínez-Colón, G. J., Ranganath, T., Zhao, N. Q., Taylor, S., Becker, W. R., et al. (2021) · The Journal of Experimental Medicine · doi:10.1084/jem.20210582 · Cited by 208 · see citing works
“For example, an agonist of a neutrophil-expressed inhibitory receptor Siglec-10 (SACCOVID) has shown promising results in suppressing hyperinflamma-tion in severe COVID-19 and is in a phase III clinical trial (Tian et al., 2018, 2020; Chen et al., 2009).”
Novel insights into the function of CD24 : A driving force in cancer
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“The CD24 and Siglec-10 axis selectively apparently repressed tissue damage-induced immune responses.(44) The sialic-acid-based pattern recognition may discriminate infections from tissue injuries.”
BackgroundInfluentialRomero, R. J., Chaiworapongsa, T., Savasan, Z. A., Xu, Y., Hussein, Y., Dong, Z., Kusanovic, J. P., Kim, C. J., & Hassan, S. S. (2011) · The Journal of Maternal-Fetal & Neonatal Medicine · doi:10.3109/14767058.2011.591460 · Cited by 213 · see citing works
“These molecules include thrombomodulin [175–177], CD24 and Siglec-10 [178,179], as well as heat shock protein-72 [180].”
BackgroundProcesses of Sterile Inflammation
Shen, H., Kreisel, D., & Goldstein, D. R. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1301539 · Cited by 208 · see citing works
Phagocytosis of Necrotic Debris at Sites of Injury and Inflammation
Westman, J., Grinstein, S., & Marques, P. E. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2019.03030 · Cited by 206 · see citing works
“It interacts with Siglec-10 in leukocytes to dampen inflammation in a variety of diseases (191).”
BackgroundLaubli, H. P., & Varki, A. P. (2019) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-019-03288-x · Cited by 205 · see citing works
T cell regulation mediated by interaction of soluble CD52 with the inhibitory receptor Siglec-10
Bandala‐Sanchez, E., Zhang, Y., Reinwald, S., Dromey, J. A., Lee, B.-H., Qian, J., Böhmer, R. M., & Harrison, L. C. (2013) · Nature Immunology · doi:10.1038/ni.2610 · Cited by 199 · see citing works
Toll-Like Receptor 9 Inhibition Confers Protection From Liver Ischemia–Reperfusion Injury
Bamboat, Z. M., Balachandran, V. P., Ocuin, L. M., Obaid, H., Plitas, G., & DeMatteo, R. P. (2009) · Hepatology · doi:10.1002/hep.23365 · Cited by 199 · see citing works
Amelioration of sepsis by inhibiting sialidase-mediated disruption of the CD24-SiglecG interaction
Chen, G., Chen, X., King, S., Cavassani, K. A., Cheng, J., Zheng, X., Cao, H., Yu, H., Qu, J., Fang, D., et al. (2011) · Nature Biotechnology · doi:10.1038/nbt.1846 · Cited by 190 · see citing works
“, our recent studies have indicated that the host response to DAMPs is negatively regulated by interactions of CD24 with SiglecG (mouse) or SIGLEC10 (the human homolog of mouse SiglecG”
BackgroundSelf-citationAlleviation of Neurotoxicity by Microglial Human Siglec-11
Wang, Y., & Neumann, H. (2010) · Journal of Neuroscience · doi:10.1523/jneurosci.3940-09.2010 · Cited by 190 · see citing works
Wang, X., Sun, R., Wei, H., & Tian, Z. (2012) · Hepatology · doi:10.1002/hep.25982 · Cited by 186 · see citing works
“Blocking HMGB1 with monoclonal antibodies (mAbs) attenuates liver injury.(29) In addition to acetaminophen-induced liver injury, HMGB1 also contributes to other liver diseases.”
BackgroundHigh‐mobility group box‐1 in sterile inflammation
Tsung, A., Tohme, S., & Billiar, T. R. (2014) · Journal of Internal Medicine · doi:10.1111/joim.12276 · Cited by 187 · see citing works
Cancer and Innate Immune System Interactions
Liu, Y., & Zeng, G. (2012) · Journal of Immunotherapy · doi:10.1097/cji.0b013e3182518e83 · Cited by 185 · see citing works
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B‐1 cells in the bone marrow are a significant source of natural IgM
Choi, Y. S., Dieter, J. A., Rothaeusler, K., Luo, Z. L., & Baumgarth, N. (2011) · European Journal of Immunology · doi:10.1002/eji.201141890 · Cited by 184 · see citing works
Conventional DCs reduce liver ischemia/reperfusion injury in mice via IL-10 secretion
Bamboat, Z. M., Ocuin, L. M., Balachandran, V. P., Obaid, H., Plitas, G., & DeMatteo, R. P. (2010) · Journal of Clinical Investigation · doi:10.1172/jci40008 · Cited by 183 · see citing works
New perspectives on the biology of acute GVHD
Paczesny, S., Hanauer, D. A., Sun, Y., & Reddy, P. R. (2009) · Bone Marrow Transplantation · doi:10.1038/bmt.2009.328 · Cited by 180 · see citing works
Human Intestinal Ischemia-Reperfusion–Induced Inflammation Characterized
Grootjans, J., Lenaerts, K., Derikx, J. P. M., Matthijsen, R. A., de Bruïne, A. P., van Bijnen, A. A., van Dam, R. M., Dejong, C. H. C., & Buurman, W. A. (2010) · The American Journal of Pathology · doi:10.2353/ajpath.2010.091069 · Cited by 186 · see citing works
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Innate Immune Regulations and Liver Ischemia-Reperfusion Injury
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EGCG stimulates autophagy and reduces cytoplasmic HMGB1 levels in endotoxin-stimulated macrophages
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“Indeed, substantial evidence has supported HMGB1 as an alarmin signal that serves to alert, recruit, and activate innate immune cells [12–14], thereby sustaining an injurious inflammatory response in sepsis [15,16].”
Duong, B. H., Tian, H., Ota, T., Completo, G. C. J., Han, S., Vela, J. L., Ota, M., Kubitz, M., Bovin, N. V., Paulson, J. C., et al. (2009) · The Journal of Experimental Medicine · doi:10.1084/jem.20091873 · Cited by 171 · see citing works
Cao, H., & Crocker, P. R. (2010) · Immunology · doi:10.1111/j.1365-2567.2010.03368.x · Cited by 172 · see citing works
HMGB1: The Central Cytokine for All Lymphoid Cells
Li, G., Liang, X., & Lotze, M. T. (2013) · Frontiers in Immunology · doi:10.3389/fimmu.2013.00068 · Cited by 167 · see citing works
“…(TLR)2, TLR4, TIM-3, chemokine CXC receptor (CXCR)4, CD24-Siglec G/10 (Park et al., 2004, 2006; Dumitriu et al., 2005; Lotze and Tracey, 2005; Bianchi, 2009; Chen et al., 2009; Tang and Lotze, 2012; Tang et al., 2012; Yanai et al., 2012), and TLR-9 when combined with DNA (Tian et al., 2007).”
BackgroundHow the Innate Immune System Senses Trouble and Causes Trouble
Hato, T., & Dagher, P. C. (2014) · Clinical Journal of the American Society of Nephrology · doi:10.2215/cjn.04680514 · Cited by 167 · see citing works
“Instead, these DAMPs are believed to induce small structural changes in other molecules that activate the receptor and its downstream pathway (28).”
BackgroundSialic Acid Mimetics to Target the Sialic Acid–Siglec Axis
Büll, C., Heise, T., Adema, G. J., & Boltje, T. J. (2016) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2016.03.007 · Cited by 165 · see citing works
PGE2 induced in and released by dying cells functions as an inhibitory DAMP
Hangai, S., Ao, T., Kimura, Y., Matsuki, K., Kawamura, T., Negishi, H., Nishio, J., Kodama, T., Taniguchi, T., & Yanai, H. (2016) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1602023113 · Cited by 162 · see citing works
“For example, aDAMPs were reported to recruit CD24–Siglec G/10 and Siglec G/10-associated phosphatases, such as SHP1, to repress TLR-mediated or Nod-like receptormediated signaling (34).”
BackgroundActivation of immune signals during organ transplantation
Li, Q., & Lan, P. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01377-9 · Cited by 173 · see citing works
“CD24 and Siglec-10 associate to negatively regulate the stimulatory activity of HSP70, HSP90, and HMGB1, and inhibit the activation of NF-κB to protect the host from the fatal response of pathological cell death.(151) This may be a potential target to protect against graft immune damage.”
BackgroundImmunological Significance of HMGB1 Post-Translational Modification and Redox Biology
Kwak, M. S., Kim, H. S., Lee, B., Kim, Y. H., Son, M., & Shin, J. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.01189 · Cited by 166 · see citing works
“In contrary, HMGB1-CD24 complex selectively represses the tissue damage-induced inflammation via interaction with Siglec-10 protein (36).”
BackgroundHigh Mobility Group Box-1 (HMGB1) Participates in the Pathogenesis of Alcoholic Liver Disease (ALD)
Ge, X., Antoine, D. J., Lu, Y., Arriazu, E., Leung, T.-M., Klepper, A. L., Branch, A. D., Fiel, M. I., & Nieto, N. (2014) · Journal of Biological Chemistry · doi:10.1074/jbc.m114.552141 · Cited by 160 · see citing works
Sweet escape: Sialic acids in tumor immune evasion
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Kim, T. S., Gorski, S. A., Hahn, S., MURPHY, K. M. M., & Braciale, T. J. (2014) · Immunity · doi:10.1016/j.immuni.2014.02.004 · Cited by 156 · see citing works
“Impor- tantly, the expression of HMGB1 on the total migrant RDCs directly paralleled the level of expression of CD24 (Figure 7C), consistent with the earlier finding that CD24 is a prominent receptor for HMGB1 (Chen et al., 2009).”
Influential
- Authors
- Chen, G.-Y., Tang, J., Zheng, P., & Liu, Y.
- Affiliations
- Chinese Academy of Sciences (CN)
- Corresponding author
- Zheng, Pan
- Liu, Yang
- Venue
- Science
- Published
- 2009-03-27
- Volume
- 323
- Issue
- 5922
- Pages
- 1722-1725
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- 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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