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CD24-Siglec G/10 discriminates danger- from pathogen-associated molecular patterns
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It is now well accepted that the innate immune system recognizes both damage (or danger)- and pathogen-associated molecular patterns (DAMP and PAMP, respectively) through pattern recognition receptors, such as Toll-like receptors (TLR) and/or Nod-like receptors (NLR). Less clear are whether and how the response to PAMP and DAMP are regulated differentially. The answers may reveal whether the primary goal of the immune system is to defend against infections or to alert the host of tissue injuries. We demonstrated recently that the host response to DAMP is controlled by a DAMP-CD24-Siglec axis. Here we propose a key role for the CD24-Siglec pathway in discriminating between DAMPs and PAMPs.
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“This may provide one mechanism by which the host immune system can modulate responses to DAMPs and distinguish DAMPs from PAMPs107.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [107]
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“Subsequently it has indeed been shown that that among others ATP, mammalian double stranded DNA and uric acid crystals activate an inflammatory response [8].”
Emerging Therapeutic Modalities against COVID-19
Malik, S., Gupta, A., Zhong, X., Rasmussen, T. P., Manautou, J. E., & Bahal, R. (2020) · Pharmaceuticals · doi:10.3390/ph13080188 · Cited by 27
The Role of Siglec-G on Immune Cells in Sepsis
Royster, W., Wang, P., & Aziz, M. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.621627 · Cited by 24
“In addition to a nuclear DAMP like HMGB1, DCs also respond to cytoplasmic DAMPs such as HSP70 and HSP90 through a TLR-dependent pathway (12, 49).”
BackgroundChristian, S. L. (2022) · OncoTargets and Therapy · doi:10.2147/ott.s366625 · Cited by 24
“CD24 acts as a co-stimulatory molecule for T cells(10) and regulates dendritic cell activation in response to danger-associated molecular patterns (DAMPs).(11,12) CD24 is constitutively expressed in erythrocytes where it decreases aggregation and promotes their half-life in circulation in mice(13) but does not appear…”
BackgroundInfluentialLiang, J., Bi, G., Huang, X., Xu, Z., Huang, Y., Bian, Y., Shan, G., Guo, W., Yan, Y., Sui, Q., et al. (2025) · 癌症：英文版 · doi:10.1002/cac2.70068 · Cited by 29
“The CD24 and SIGLEC protein family signaling axis has been extensively demonstrated to be an innate immune checkpoint regulating host response to tissue injuries [35–37].”
Epithelial dysregulation in obese severe asthmatics with gastro-oesophageal reflux
Perotin, J., Schofield, J. P. R., Wilson, S. J., Ward, J., Brandsma, J., Strazzeri, F., Bansal, A. T., Yang, X., Rowe, A., Corfield, J., et al. (2019) · European Respiratory Journal · doi:10.1183/13993003.00453-2019 · Cited by 23
“0004), a cell surface receptor involved in suppression of immune responses to DAMPs (12), organization of tight”
BackgroundInfluentialYin and yang of tumor inflammation: How innate immune suppressors shape the tumor microenvironments
Jinushi, M. (2013) · International Journal of Cancer · doi:10.1002/ijc.28626 · Cited by 22
“Siglec-G belongs to a family of immunoglobulinlike lectins that contain ITIM motifs and associate with SHP2 and transduces signals to inhibit innate and B cell-dependent immune responses.(80,81) Moreover, Siglec-G expression is upregulated on macrophages by RNA virus-dependent NFkappaB signals.”
BackgroundEhira, N., Oshiumi, H., Matsumoto, M., Kondo, T., Asaka, M., & Seya, T. (2010) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/1756-9966-29-135 · Cited by 21
“Yet the GDF3-CD24 pathway frequently turns positive when the cells are malignantly transformed [37] which may support the notion that CD24, when complexed with other molecules, alters its function for discrimination of danger signals [37].”
BackgroundTLR1 expression in mouse brain was increased in a KA-induced seizure model
Wang, F.-X., Liu, S., Zheng, X., Chen, X., Lu, L.-X., Chen, B., Xiong, X., Shu, H., Yang, Q., & Yang, H. (2015) · Inflammation Research · doi:10.1007/s00011-015-0828-7 · Cited by 21
Agents of cancer immunosurveillance: HSPs and dsDNA
Nayak, D. A., & Binder, R. J. (2022) · Trends in Immunology · doi:10.1016/j.it.2022.03.004 · Cited by 22
Unravelling CD24 ‐ Siglec‐10 pathway: Cancer immunotherapy from basic science to clinical studies
Hazra, R., Chattopadhyay, S., Mallick, A., Gayen, S., & Roy, S. (2024) · Immunology · doi:10.1111/imm.13847 · Cited by 20
“Nevertheless, numerous studies indicate that the human Siglec-10 partners (recognized as the murine Siglec-G homologue) along with CD24 recognize endogenous damage-associated molecular patterns (DAMPs) and hinder DAMP-induced innate inflammatory reactions [97].”
Inflammaging as the basis of age-associated diseases
Artemyeva, O. V., & Gankovskaya, L. V. (2020) · Medical Immunology (Russia) · doi:10.15789/1563-0625-iat-1938 · Cited by 21
Molina, L. D. P., López‐Granados, E., Lécrevisse, Q., Torres, J. M., Pérez‐Andrés, M., Blanco, E., Wentink, M. W. J., Bonroy, C., Nechvátalová, J., Milota, T., et al. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2020.603972 · Cited by 20
“CD24 is also highly expressed on immature B-cells and it is associated with Siglec-10 that interacts with SHP-1 phosphatases, a complex implicated in NFkB activation and the prevention of signaling from non-specific antigen receptors (47).”
BackgroundA hypermorphic SP1-binding CD24 variant associates with risk and progression of multiple sclerosis.
Wang, L., Liu, R., Li, D., Lin, S., Fang, X., Backer, G., Kain, M., Rammoham, K., Zheng, P., & Liu, Y. (2012) · Europe PMC (PubMed Central) · Cited by 19
Self-citationHigh Mobility Group Box Protein-1 in Wound Repair
Ranzato, E., Martinotti, S., Pedrazzi, M., & Patrone, M. (2012) · Cells · doi:10.3390/cells1040699 · Cited by 19
Schäck, L. M., Büettner, M., Wirth, A., Neunaber, C., Krettek, C., Hoffmann, A., & Noack, S. (2015) · Stem Cells International · doi:10.1155/2016/1319578 · Cited by 19
“CD24 can interact with nucleolin, a ubiquitous protein that can function as a nuclear shuttle protein opening the possibility that nucleolin might facilitate the nuclear import of CD24 in hBMSCs [17].”
Immune Cell Circuits in Mucosal Wound Healing: Clinical Implications
Zundler, S., Tauschek, V., & Neurath, M. F. (2020) · Visceral Medicine · doi:10.1159/000506846 · Cited by 19
The role of danger signals and ectonucleotidases in acute graft-versus-host disease
Apostolova, P., & Zeiser, R. (2016) · Human Immunology · doi:10.1016/j.humimm.2016.02.005 · Cited by 19
Li, D., Hu, M., Liu, Y., Du, P., Du, P., Li, C.-S., Cheng, L., Liu, P., Jiang, J., Su, L., et al. (2018) · Cell Discovery · doi:10.1038/s41421-017-0007-9 · Cited by 18
Self-citationDevelopmental trajectory of extracellular vesicle characteristics from the lungs of preterm infants
Ransom, M. A., Bunn, K. E., Negretti, N. M., Jetter, C. S., Bressman, Z. J., Sucre, J. M. S., & Pua, H. H. (2023) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00389.2022 · Cited by 17
Green, O., Shenberg, G., Baruch, R., Argaman, L., Levin, T., Michelson, I., Hadary, R., Isakovich, B., Golos, M., Schwartz, R., et al. (2023) · Biomedicines · doi:10.3390/biomedicines11092523 · Cited by 17
“CD24, Siglec 10, and HMGB1 form a trimolecular complex that exerts negative regulation on the NF-kB pathway [10,13,14].”
IAPs protect host target tissues from graft-versus-host disease in mice
Toubai, T., Rossi, C., Oravecz-Wilson, K. I., Liu, C., Zajac, C. K., Wu, S.-R. J., Sun, Y., Fujiwara, H., Tamaki, H., Peltier, D., et al. (2017) · Blood Advances · doi:10.1182/bloodadvances.2017004242 · Cited by 17
Inhaled CD24-Enriched Exosomes (EXO-CD24) as a Novel Immune Modulator in Respiratory Disease
Shapira, S., Schwartz, R., Tsiodras, S., Bar‐Shai, A., Melloul, A., Borsekofsky, S., Peer, M., Adi, N., MacLoughlin, R. J., & Arber, N. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms25010077 · Cited by 15
“…between Damage-Associated Molecular Patterns (DAMPs), which are endogenous molecules that are constitutively expressed and released upon tissue damage or stress from damaged or dying cells, and Pathogen-Associated Molecular Patterns (PAMPs), molecular structures produced by microorganisms [13–15].”
BackgroundPeriodontitis Risk Variants at SIGLEC5 Impair ERG and MAFB Binding
Mueller, R., Chopra, A., Dommisch, H., & Schäefer, A. S. (2021) · Journal of Dental Research · doi:10.1177/00220345211049984 · Cited by 15
“As a result, DAMPs and PAMPs would become indistinguishable, which could provide an explanation for massive inflammation and tissue destruction (Liu et al. 2009), as typically seen in severe periodontitis phenotypes (stage III) with a rapid rate of progression (grade C).”
BackgroundThe Big Potential of Small Particles: Lipid-Based Nanoparticles and Exosomes in Vaccination
Shimon, M. B., Shapira, S., Seni, J., & Arber, N. (2022) · Vaccines · doi:10.3390/vaccines10071119 · Cited by 18
“CD24 binds Siglec-10, resulting in an activation of the Siglec-10 signaling pathway [66,67].”
BackgroundThe Hypothesis on Function of Glycosphingolipids and ABO Blood Groups Revisited
Kościelak, J. (2012) · Neurochemical Research · doi:10.1007/s11064-012-0734-0 · Cited by 15
Myeloid dysregulation and therapeutic intervention in COVID-19
Gu, R., Mao, T., Qiao, L., Su, T. T., & Wang, J. (2021) · Seminars in Immunology · doi:10.1016/j.smim.2021.101524 · Cited by 14
“CD24 represses DAMP-induced immunity by directly trapping DAMPs to prevent agonistic receptor binding and/or by actively suppressing downstream signaling pathways through Siglec-10/G receptor [74,75].”
Surprising magic of CD24 beyond cancer
He, W., Shi, P., Shi, X., Lv, Y., Xie, H., & Hai, Z. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1334922 · Cited by 14
“The primary and most in fl uential category includes molecular patterns related to pathogens, known as PAMPs, while the secondary category, which is of lesser importance, contains molecular patterns associated with damage, known as DAMPs (87, 88).”
BackgroundInfluentialThaxton, J. E., Liu, B., Zheng, P., Liu, Y., & Li, Z. (2014) · The Journal of Immunology · doi:10.4049/jimmunol.1302755 · Cited by 14
“recruitment of the ITIM Siglec10/G and subsequent abrogation of inflammatory cytokine signals through blockade of NF-kB activation (7).”
BackgroundSelf-citationCD24Fc ameliorates immune-related adverse events while preserving anti-tumor therapeutic effect
Liu, M., Wang, X., Du, X., Zhang, Y., Ai, C., Hu‐Lieskovan, S., Li, T., Devenport, M., Liu, Y., & Zheng, P. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-01030-x · Cited by 14
Self-citationKedarinath, K., Fox, C. R., Crowgey, E. L., Mazar, J., Phelan, P. E., Westmoreland, T. J., Alexander, K. A., & Parks, G. D. (2022) · Viruses · doi:10.3390/v14081735 · Cited by 14
Chen, X., Li, H., Song, H., Wang, J., Zhang, X., Han, P., & Wang, X. (2022) · Journal of Extracellular Vesicles · doi:10.1002/jev2.12288 · Cited by 12
“While CD24 inhibits immune activation induced by damage-associated molecular patterns (DAMPs), this activation neither affects immune recognition of pathogen-associated molecular patterns (PAMPs) nor interferes with virus clearance (Liu et al., 2009).”
BackgroundAn overview of some potential immunotherapeutic options against COVID-19
Bayat, M., Asemani, Y., Mohammadi, M. R., Sanaei, M., Namvarpour, M., & Eftekhari, R. (2021) · International Immunopharmacology · doi:10.1016/j.intimp.2021.107516 · Cited by 11
Tsioulos, G., Grigoropoulos, I., Moschopoulos, C. D., Shapira, S., Poulakou, G., Antoniadou, A., Boumpas, D. T., Arber, N., & Tsiodras, S. (2022) · Life · doi:10.3390/life12101472 · Cited by 12
“CD24’s link to DAMPs prevents them from binding to the TLRs, therefore inhibiting the NF-kB pathway, an extremely significant signaling pathway, that induces the production of cytokines and chemokines [15,31].”
Background
Metadata
- Authors
- Liu, Y., Chen, G.-Y., & Zheng, P.
- Affiliations
- University of Michigan (US)
- Corresponding author
- Liu, Yang
- Venue
- Trends in Immunology
- Publisher
- Elsevier BV
- Published
- 2009-12
- Volume
- 30
- Issue
- 12
- Pages
- 557-561
- ISSN
- 1471-4906 (ISSN-L)
- PMC
- PMC2788100
- OpenAlex
- W1979054778
- Cited by
- 147
- References
- 68
- Citations by year
- 2026: 3 · 2025: 9 · 2024: 5 · 2023: 6 · 2022: 14 · 2021: 12 · 2020: 8 · 2019: 3 · 2018: 7 · 2017: 5 · 2016: 9 · 2015: 6 · 2014: 8 · 2013: 11 · 2012: 13
- FWCI
- 1.05
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5r01ai064350-15)
- National Institute on Aging (R01AG036690)
- National Cancer Institute (R01CA112001, CA-58033, R01CA058033)
- National Institute of General Medical Sciences (RC1GM091648)
- National Institute of Allergy and Infectious Diseases (R01-AI064350, AI64350)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Keywords
- CD24, Siglec-G, Siglec-10, damage-associated molecular patterns, pathogen-associated molecular patterns, innate immunity, pattern recognition receptors, Toll-like receptors, NOD-like receptors, tissue injury response
- MeSH terms
- Animals, Heat-Shock Proteins, Humans, Immunity, Innate, Lymphocyte Activation, Protein Binding, Lectins, Receptors, Pattern Recognition, Toll-Like Receptor 2, Toll-Like Receptor 4, Mice, CD24 Antigen, Nod1 Signaling Adaptor Protein, Protein Tyrosine Phosphatase, Non-Receptor Type 6, Sialic Acid Binding Immunoglobulin-like Lectins
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