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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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“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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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BackgroundInfluentialSelf-citationNatural ligands for CD33-related Siglecs?
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“Given the results, it is very likely that the interaction studied by these authors (Chen et al. 2009) is between the sialic acid-binding site of Siglec-10 and the heavily sialylated glycans of CD24.”
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BackgroundThe new progress in cancer immunotherapy
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“Previously, we found that interaction between CD24 and Siglec-G/10 is a key regulator of polybacterial sepsis, and this interaction requires sialylation of CD24 (24, 25).”
BackgroundSelf-citationChang, X., Obianwuna, U. E., Wang, J., Zhang, H., Qi, G., Qiu, K., & Wu, S. (2023) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2023.123855 · Cited by 32
The biological roles of CD24 in ovarian cancer: old story, but new tales
Gu, Y., Zhou, G., Tang, X., Shen, F., Ding, J., & Hua, K. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1183285 · Cited by 32
“CD24 could negatively regulate the stimulatory activity of high mobility group box 1, heat shock protein 70, as well as heat shock protein 90, and could inhibit the activation of nuclear factor kB (NF-kB) (13).”
BackgroundSu, Z., Lu, H., Jiang, Y., Zhu, H., Ze, L., Zhang, P., Ni, P., Shen, H., Xu, W., & Xu, H. (2015) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2015.09.037 · Cited by 33
HMGB1 in severe soft tissue infections caused by Streptococcus pyogenes
Johansson, L., Snäll, J., Sendi, P., Linnér, A., Thulin, P., Linder, A., Treutiger, C.-J., & Norrby‐Teglund, A. (2014) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2014.00004 · Cited by 32
“Several receptors have been shown to interact with HMGB1 including toll-like receptor 4 (TLR4), the receptor for advanced glycation end products (RAGE) and CD24-Siglec-10 (Lotze and Tracey, 2005; Tian et al., 2007; Chen et al., 2009).”
BackgroundCD24 Is a Potential Immunotherapeutic Target for Mantle Cell Lymphoma
Freile, J. Á., Avtenyuk, N. U., Corrales, M. G., Lourens, H. J., Huls, G. A., van Meerten, T., Cendrowicz, E., & Bremer, E. (2022) · Biomedicines · doi:10.3390/biomedicines10051175 · Cited by 32
“Although newly uncovered in the context of cancer, such immune checkpoint activity of the CD24/Siglec-10 axis on innate immune cells has been well established in the context of apoptotic cell removal and infection [49].”
BackgroundStarkova, T. Y., Polyanichko, A. M., Артамонова, Т. О., Сергеевна, Ц. А., Tomilin, A. N., & Chikhirzhina, E. V. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24043577 · Cited by 31
“Depending on the redox state, extracellular HMGB1 can (1) act as a signaling molecule by activating the MAPKs (infarct, inflammation, and post-infarct remodeling [27]), NF-kB (thrombosis [33], urothelial carcinoma [34], inflammation during tissue damage [35]) and phosphoinositide-3-kinase/AKT signaling pathways (infla…”
BackgroundShoda, L. K. M., Battista, C., Siler, S. Q., Pisetsky, D. S., Watkins, P. B., & Howell, B. A. (2017) · Gene Regulation and Systems Biology · doi:10.1177/1177625017696074 · Cited by 31
Li, W., Ling, H.-P., You, W., Liu, H., Sun, Q., Zhou, M., Shen, W., Zhao, J., Zhu, L., & Hang, C. (2013) · Molecular Neurobiology · doi:10.1007/s12035-013-8509-4 · Cited by 31
Alarmin‐induced cell migration
Yang, D., Wei, F., Tewary, P., Howard, O. M. Z., & Oppenheim, J. J. (2013) · European Journal of Immunology · doi:10.1002/eji.201243138 · Cited by 31
Purification and Immune Phenotyping of B-1 Cells from Body Cavities of Mice
Yenson, V. M., & Baumgarth, N. (2014) · Methods in molecular biology · doi:10.1007/978-1-4939-1161-5_2 · Cited by 31
Zuo, Z., Che, X., Wang, Y., Li, B., Li, J., Dai, W. H., Lin, C. P., & Huang, C. (2014) · Oncotarget · doi:10.18632/oncotarget.2150 · Cited by 30
Carreras‐González, A., Barriales, D., Palacios, A., Montesinos-Robledo, M., Navasa, N., Azkargorta, M., Peña‐Cearra, A., Tomás‐Cortázar, J., Escobés, I., Pascual‐Itoiz, M. Á., et al. (2019) · PLoS Pathogens · doi:10.1371/journal.ppat.1008163 · Cited by 29
“burgdorferi, while others, including the GPI-anchored proteins analyzed, seem to have an accessory role, possibly through their interaction with CR3 [27] and potentially, other receptors [28].”
BackgroundTajbakhsh, A., Rezaee, M., Barreto, G. E., Moallem, S. A., Henney, N. C., & Sahebkar, A. (2020) · International Immunopharmacology · doi:10.1016/j.intimp.2019.106134 · Cited by 30
Jansen, S. A., Nieuwenhuis, E. E. S., Hanash, A. M., & Lindemans, C. A. (2022) · Mucosal Immunology · doi:10.1038/s41385-022-00527-6 · Cited by 30
Role of Siglecs in viral infections: A double-edged sword interaction
Regué, D. R., Resa‐Infante, P., Gallemí, M., Laguía, F., Muñiz-Trabudua, X., Muñoz‐Basagoiti, J., Perez‐Zsolt, D., Chojnacki, J., Benet, S., Clotet, B., et al. (2022) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2022.101113 · Cited by 30
Wang, W., Sun, L., Deng, Y., & Tang, J. (2013) · FEBS Journal · doi:10.1111/febs.12132 · Cited by 30
Self-citationProkaryotic and Eukaryotic Heat Shock Proteins in Infectious Disease
Pockley, A. G., Calderwood, S. K., & Santoro, M. (2009) · Heat shock proteins · doi:10.1007/978-90-481-2976-8 · Cited by 30
HMGB1: a double-edged sword and therapeutic target in the female reproductive system
Ren, Y., Zhu, D., Han, X., Zhang, Q., Chen, B., Zhou, P., Wei, Z., Zhang, Z., Cao, Y., & Zou, H. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1238785 · Cited by 30
Welker, J., Pulido, J. D., Catanzaro, A. T., Malvestutto, C. D., Li, Z., Cohen, J. B., Whitman, E. D., Byrne, D., Giddings, O. K., Lake, J. E., et al. (2022) · The Lancet Infectious Diseases · doi:10.1016/s1473-3099(22)00058-5 · Cited by 29
Self-citationAyala, A., Elphick, G. F., Kim, Y. S., Huang, X., Carreira-Rosario, A., Santos, S. C., Shubin, N. J., Chen, Y., Reichner, J. S., & Chung, C. (2013) · Journal of Innate Immunity · doi:10.1159/000355888 · Cited by 29
Xiang, M., Yuan, Y., Fan, L., Li, Y., Li, A., Yin, L., Scott, M. J., Xiao, G., Billiar, T. R., Wilson, M. A., et al. (2012) · Shock · doi:10.1097/shk.0b013e318249b81d · Cited by 29
“HMBG1 mainly acts through RAGE rather than TLR4 to induce HPC mobilization High-mobility group box 1 has been shown to bind to at least five membrane receptors, including RAGE (20), TLR2, TLR4 (21), triggering receptor expressed on myeloid cells 1, and CD24 (22).”
BackgroundSiglec genes confer resistance to systemic lupus erythematosus in humans and mice
Flores, R., Zhang, P., Wu, W., Wang, X., Ye, P., Zheng, P., & Liu, Y. (2018) · Cellular and Molecular Immunology · doi:10.1038/cmi.2017.160 · Cited by 29
Self-citationSialoside-based pattern recognitions discriminating infections from tissue injuries
Liu, Y., Chen, G.-Y., & Zheng, P. (2011) · Current Opinion in Immunology · doi:10.1016/j.coi.2010.10.004 · Cited by 28
Self-citationExamination of the role of necroptotic damage-associated molecular patterns in tissue fibrosis
Liu, X., Lu, F., & Chen, X. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.886374 · Cited by 30
“The sialic-acid-binding immunoglobulin-like lectin-CD24 signaling pathway can inhibit DAMP-induced inflammation and weaken its proinflammatory function, particularly the secretion of TNF-a, IL-1b, and IL-6, to prevent the pathological inflammatory responses caused by cell death and necrosis (161, 162).”
BackgroundGeng, S., Lu, R., Zhang, Y., Wu, Y., Xie, L., Caldwell, B. A., Pradhan, K., Yi, Z., Hou, J., Xu, F., et al. (2024) · Circulation Research · doi:10.1161/circresaha.124.325023 · Cited by 30
“70 We observed that 4-PBA can potently and uniformly elevate CD24 levels on all monocytes, regardless of their subsets based on the conventional Ly6C levels.”
BackgroundSustained in situ protein production and release in the mammalian gut by an engineered bacteriophage
Baker, Z. R., Zhang, Y., Zhang, H., Franklin, H. C., Serpa, P. B. S., Southard, T. L., Li, L., & Hsu, B. B. (2025) · Nature Biotechnology · doi:10.1038/s41587-025-02570-7 · Cited by 29
“This structure suppresses DAMP-related inflammation 34 and has a predicted anti-inflammatory role in colitis 35 .”
Riner, D. K., Ferragine, C. E., Maynard, S. K., & Davies, S. J. A. (2013) · PLoS Pathogens · doi:10.1371/journal.ppat.1003708 · Cited by 29
“To test this hypothesis, we administered two wellcharacterized hepatotoxins, acetaminophen (AAP) or D-galactosamine (GalN), to RAG mice throughout pre-patent infection, at doses sufficient to result in hepatocellular death and inflammation [18–21], in an attempt to simulate the cell death observed in wild type mice.”
MethodMurshid, A., Borges, T. J., Bonorino, C., Lang, B. J., & Calderwood, S. K. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2019.03035 · Cited by 28
Curcumin analogue C66 attenuates obesity-induced renal injury by inhibiting chronic inflammation
Lin, Y., Hu, X., Hu, X., Yin, S., Chen, J., He, H., Hong, S., Yang, B., Singh, K. K., Feng, J., et al. (2021) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2021.111418 · Cited by 28
The Pro‐Inflammatory Role of Adiponectin at the Maternal–Fetal Interface
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Du, K., McGill, M. R., Xie, Y., & Jaeschke, H. (2015) · Food and Chemical Toxicology · doi:10.1016/j.fct.2015.10.016 · Cited by 28
“18 various DAMPs in the pathophysiology of APAP-induced liver injury also suggests that inflammatory mediators can have an impact on the intracellular mechanism of cell death (Cai et al., 2014; Chen et al., 2009; Imaeda et al., 2009; Singhal et al., 2007).”
Loss of CD24 in Mice Leads to Metabolic Dysfunctions and a Reduction in White Adipocyte Tissue
Fairbridge, N. A., Southall, T. M., Ayre, D. C., Komatsu, Y., Raquet, P. I., Brown, R., Randell, E. W., Kovács, C. S., & Christian, S. L. (2015) · PLoS ONE · doi:10.1371/journal.pone.0141966 · Cited by 28
Senescence-associated sialidase revealed by an activatable fluorescence-on labeling probe
Zhu, R., Wang, S., Xue, Z., Han, J., & Han, S. (2018) · Chemical Communications · doi:10.1039/c8cc07024e · Cited by 28
Recognition of Apoptotic Cells by Epithelial Cells
Patel, V. A., Lee, D. J., Feng, L., Antoni, A., Lieberthal, W., Schwartz, J. H., Rauch, J., Ucker, D. S., & Levine, J. S. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.m109.018440 · Cited by 27
Metadata
- 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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