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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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Novel insights into the function of CD24 : A driving force in cancer
Altevogt, P., Sammar, M., Hüser, L., & Kristiansen, G. (2020) · International Journal of Cancer · doi:10.1002/ijc.33249 · Cited by 223
“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 215
“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 214
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 214
“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
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
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
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
“, 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
Wang, X., Sun, R., Wei, H., & Tian, Z. (2012) · Hepatology · doi:10.1002/hep.25982 · Cited by 188
“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
Cancer and Innate Immune System Interactions
Liu, Y., & Zeng, G. (2012) · Journal of Immunotherapy · doi:10.1097/cji.0b013e3182518e83 · Cited by 189
Self-citationRicketts, T. D., Prieto‐Domínguez, N., Gowda, P. S., & Ubil, E. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.642285 · Cited by 186
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
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 188
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 187
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
Paudel, Y. N., Angelopoulou, E., Piperi, C., Balasubramaniam, V. R. M. T., Othman, I., & Shaikh, M. F. (2019) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2019.172487 · Cited by 181
Innate Immune Regulations and Liver Ischemia-Reperfusion Injury
Lü, L., Zhou, H., Ni, M., Wang, X., Busuttil, R. W., Kupiec‐Weglinski, J. W., & Zhai, Y. (2016) · Transplantation · doi:10.1097/tp.0000000000001411 · Cited by 176
EGCG stimulates autophagy and reduces cytoplasmic HMGB1 levels in endotoxin-stimulated macrophages
Li, W., Zhu, S., Li, J., Assa, A., Jundoria, A., Xu, J., Fan, S., Eissa, N. T., Tracey, K. J., Sama, A. E., et al. (2011) · Biochemical Pharmacology · doi:10.1016/j.bcp.2011.02.015 · Cited by 172
“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 174
Cao, H., & Crocker, P. R. (2010) · Immunology · doi:10.1111/j.1365-2567.2010.03368.x · Cited by 172
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 171
“…(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 184
“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
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 168
“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 175
“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 167
“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
Sweet escape: Sialic acids in tumor immune evasion
Büll, C., den Brok, M. H., & Adema, G. J. (2014) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2014.07.005 · Cited by 158
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
“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
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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