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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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Citations
Cites
A human homologue of the Drosophila Toll protein signals activation of adaptive immunity
Medzhitov, R., Preston-Hurlburt, P., & Janeway, C. A. J. (1997) · Nature · doi:10.1038/41131 · Cited by 6,137
Tolerance, Danger, and the Extended Family
Matzinger, P. (1994) · Annual Review of Immunology · doi:10.1146/annurev.iy.12.040194.005015 · Cited by 4,848
Release of chromatin protein HMGB1 by necrotic cells triggers inflammation
Scaffidi, P., Misteli, T., & Bianchi, M. E. (2002) · Nature · doi:10.1038/nature00858 · Cited by 4,221
Approaching the asymptote? Evolution and revolution in immunology.Preprint
Janeway, C. (1989) · Cold Spring Harbor Symposia on Quantitative Biology · doi:10.1101/sqb.1989.054.01.003 · Cited by 3,396
HMG-1 as a Late Mediator of Endotoxin Lethality in Mice
Wang, H., Bloom, O., Zhang, M., Vishnubhakat, J. M., Ombrellino, M., Che, J., Frazier, A., Yang, H., Ivanova, S., Borovikova, L. V., et al. (1999) · Science · doi:10.1126/science.285.5425.248 · Cited by 3,386
Yang, Y., Li, S., Yang, Q., Shi, Y., Zheng, M., Liu, Y., Chen, F., Song, G., Xu, H., Wan, T., et al. (2014) · Cellular Physiology and Biochemistry · doi:10.1159/000358696 · Cited by 3,263
Self-citationApetoh, L., Ghiringhelli, F., Tesniere, A., Obeid, M., Ortiz, C., Criollo, A., Mignot, G., Maiuri, M. C., Ullrich, E., Saulnier, P., et al. (2007) · Nature Medicine · doi:10.1038/nm1622 · Cited by 3,056
Siglecs and their roles in the immune system
Crocker, P. R., Paulson, J. C., & Varki, A. P. (2007) · Nature reviews. Immunology · doi:10.1038/nri2056 · Cited by 2,032
Park, J. S., Svetkauskaite, D., He, Q., Kim, J., Strassheim, D., Ishizaka, A., & Abraham, E. H. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m306793200 · Cited by 1,582
Tian, J., Avalos, A. M., Mao, S.-Y., Chen, B., Senthil, K., Wu, H., Parroche, P., Drabic, S., Golenbock, D., Sirois, C., et al. (2007) · Nature Immunology · doi:10.1038/ni1457 · Cited by 1,372
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Items 101–200 of 790
Delen, M. V., Derdelinckx, J., Wouters, K., Nelissen, I., & Cools, N. (2024) · Journal of Extracellular Vesicles · doi:10.1002/jev2.12458 · Cited by 156
Anti-Inflammatory Role of Fetuin-A in Injury and Infection
Wang, H., & Sama, A. (2012) · Current Molecular Medicine · doi:10.2174/156652412800620039 · Cited by 152
“These innate immune cells are equipped with pattern recognition receptors (such as TLR2, TLR4, and TLR9) [1–3] that can recognize both pathogen- and damage-associated molecular patterns (PAMPs, such as endotoxin, and DAMPs, such as HMGB1) [4–7].”
Chen, G., Brown, N. K., Wu, W., Khedri, Z., Yu, H., Chen, X., van de Vlekkert, D., d’Azzo, A., Zheng, P., & Liu, Y. (2014) · eLife · doi:10.7554/elife.04066 · Cited by 153
“Consistent with its intracellular ITIM- or ITIM-like motifs, engagement of Siglec-G with its natural ligands has been shown to inhibit both innate immune responses and adaptive T cell responses (Chen et al., 2009; BandalaSanchez et al., 2013; Toubai et al., 2014).”
BackgroundResultInfluentialSelf-citationLü, B., Wang, C., Wang, M., Li, W., Chen, F., Tracey, K. J., & Wang, H. (2014) · Expert Review of Clinical Immunology · doi:10.1586/1744666x.2014.909730 · Cited by 153
“HMGB1 interacts with a family of cell surface receptors and binding proteins including RAGE [48], TLR4 [53], TLR9 [6,48], cluster of differentiation 24/Siglec-10 [54], Mac-1 [51], thrombomodulin [55] as well as single transmembrane domain proteins (e.”
BackgroundInfluence of microbial environment on autoimmunity
Chervonsky, A. V. (2009) · Nature Immunology · doi:10.1038/ni.1801 · Cited by 168
“Under sterile conditions, however, the possible pathogen-induced molecular pattern activity of HMGB1 and of other DAMPs is inhibited by CD24–Siglec complexe”
BackgroundYang, D., Postnikov, Y. V., Li, Y., Tewary, P., de la Rosa, G., Wei, F., Klinman, D. M., Gioannini, T. L., Weiss, J. P., Furusawa, T., et al. (2011) · The Journal of Experimental Medicine · doi:10.1084/jem.20101354 · Cited by 149
“All alarmins identified so far, such as defensins, cathelicidins, eosinophil derived neurotoxin, granulysin, and HMGB1 (highmobility group box 1) protein, have been shown to enhance inflammation, anti microbial defense, adaptive immunity, and wound healing (Wang et al., 1999; RovereQuerini et al., 2004; Kurosaka e…”
BackgroundInfluentialGut mucosal DAMPs in IBD: from mechanisms to therapeutic implications
Boyapati, R. K., Rossi, A. G., Satsangi, J., & Ho, G. (2016) · Mucosal Immunology · doi:10.1038/mi.2016.14 · Cited by 150
“In contrast to the upregulating effects of TREM-1, CD24-Siglec signaling (Siglec-G in mice; Siglec-10 in humans) has been shown to suppress DAMP-related but not PAMP-related inflammation.(123) Siglecs (sialic acid-binding immunoglobulin-like lectins) are members of the Ig superfamily that bind with CD24 and selectivel…”
BackgroundSiglec-15 as an Emerging Target for Next-generation Cancer Immunotherapy
Sun, J., Qiao, L., Sanmamed, M. F., & Wang, J. (2020) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-19-2925 · Cited by 149
“CD24Fc is a fusion protein developed by OncoImmune, of which one portion interacts with Siglec-10 on macrophages and dendritic cells and results in immune inhibition via a SHP-1– mediated pathway (55, 56).”
BackgroundCD24-Siglec G/10 discriminates danger- from pathogen-associated molecular patterns
Liu, Y., Chen, G.-Y., & Zheng, P. (2009) · Trends in Immunology · doi:10.1016/j.it.2009.09.006 · Cited by 147
Self-citationCD22 and Siglec‐G: B‐cell inhibitory receptors with distinct functions
Nitschke, L. (2009) · Immunological Reviews · doi:10.1111/j.1600-065x.2009.00801.x · Cited by 147
“A recent study reported a sialic acid-dependent interaction of the glycosylated cell surface molecule CD24 with Siglec-G and soluble high mobility group box 1 protein (HMGB1) in a tri-molecular complex on other cells than B cells (114).”
BackgroundMacrophage‐Mediated Tumor Cell Phagocytosis: Opportunity for Nanomedicine Intervention
Zhou, X., Liu, X., & Huang, L. (2020) · Advanced Functional Materials · doi:10.1002/adfm.202006220 · Cited by 147
Clinical landscape of macrophage-reprogramming cancer immunotherapies
Rannikko, J. H., & Hollmén, M. (2024) · British Journal of Cancer · doi:10.1038/s41416-024-02715-6 · Cited by 169
“Further development should consider other immune-and cancer-related functions of CD24 and additional CD24 and Siglec-10 ligands binding to different glycosylated protein forms [79, 81, 82].”
A Hepatic Protein, Fetuin-A, Occupies a Protective Role in Lethal Systemic Inflammation
Li, W., Zhu, S., Li, J., Huang, Y., Rongrong, Z., Fan, X., Yang, H., Gong, X., Eissa, N. T., Jahnen‐Dechent, W., et al. (2011) · PLoS ONE · doi:10.1371/journal.pone.0016945 · Cited by 143
“damage-associated molecular patterns (DAMPs, such as HMGB1) [3,4,7,8].”
BackgroundHigh-mobility group box family of proteins: ligand and sensor for innate immunity
Yanai, H., Ban, T., & Taniguchi, T. (2012) · Trends in Immunology · doi:10.1016/j.it.2012.10.005 · Cited by 146
Targeting HMGB1 in the treatment of sepsis
Wang, H., Ward, M. F., & Sama, A. E. (2014) · Expert Opinion on Therapeutic Targets · doi:10.1517/14728222.2014.863876 · Cited by 144
“In addition, HMGB1 can bind to multiple cell surface receptors including RAGE [59], TLR2, TLR4 [60-62], TLR9 [21,59], cluster of differentiation 24 (CD24)/Siglec-10 [63], Mac-1 [56], thrombomodulin [64], as well as single transmembrane domain proteins (e.”
BackgroundKanellakis, P., Agrotis, A., Kyaw, T. S., Koulis, C., Ahrens, I., Mori, S., Takahashi, H. K., Liu, K., Peter, K., Nishibori, M., et al. (2010) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.110.218669 · Cited by 144
Targeting sialic acid–Siglec interactions to reverse immune suppression in cancer
Adams, O. J., Stanczak, M. A., von Gunten, S., & Laubli, H. P. (2017) · Glycobiology · doi:10.1093/glycob/cwx108 · Cited by 142
Ge, X., Arriazu, E., Magdaleno, F., Antoine, D. J., Cruz, R. D., Theise, N. D., & Nieto, N. (2018) · Hepatology · doi:10.1002/hep.30093 · Cited by 142
“Among the receptors HMGB1 binds to, RAGE and TLR4 are expressed in HSC and participate in liver fibrosis (22-34).”
Overcoming Wnt–β-catenin dependent anticancer therapy resistance in leukaemia stem cells
Perry, J. M., Fang, T., Roy, A., Lin, T. L., He, X., Chen, S., Lü, X., Nemechek, J. M., Ruan, L., Yu, X., et al. (2020) · Nature Cell Biology · doi:10.1038/s41556-020-0507-y · Cited by 140
Emerging strategies in targeting tumor-resident myeloid cells for cancer immunotherapy
Wang, Y., Johnson, K. C. C., Gatti-Mays, M. E., & Li, Z. (2022) · Journal of Hematology & Oncology · doi:10.1186/s13045-022-01335-y · Cited by 137
Next frontier in tumor immunotherapy: macrophage-mediated immune evasion
Qiu, Y., Chen, T., Hu, R., Zhu, R., Li, C., Ruan, Y., Xie, X., & Li, Y. (2021) · Biomarker Research · doi:10.1186/s40364-021-00327-3 · Cited by 138
“CD24, also called heat stable antigen, is a highly glycosylated surface protein anchored by glycosylphosphatidylinositol, which could interact with sialic acid-binding immunoglobulin-like lectin-10 (Siglec-10) to reduce the innate immune-mediated noxious inflammation caused by infection or liver damage [26].”
BackgroundWilliams, C. D., Bajt, M. L., Farhood, A. I., & Jaeschke, H. (2010) · Liver International · doi:10.1111/j.1478-3231.2010.02284.x · Cited by 130
“high mobility group box proteins (30, 52), suggest this is a classical scenario of a sterile inflammatory response.”
BackgroundEmerging Role of High-Mobility Group Box 1 (HMGB1) in Liver Diseases
Chen, R., Hou, W., Zhang, Q., Kang, R., Fan, X., & Tang, D. (2013) · Molecular Medicine · doi:10.2119/molmed.2013.00099 · Cited by 130
Danger Signals in the Initiation of the Inflammatory Response after Myocardial Infarction
de Haan, J. J., Smeets, M. B., Pasterkamp, G., & Arslan, F. (2013) · Mediators of Inflammation · doi:10.1155/2013/206039 · Cited by 139
“Interaction with coreceptors like CD24-Siglec-G/-10 [3] or CD14/MD2 [4] allows the PRRs to discriminate between DAMPs and PAMPs and subsequently influence the level of inflammation [5].”
BackgroundRegulation of B Cell Functions by the Sialic Acid-Binding Receptors Siglec-G and CD22
Jellusova, J., & Nitschke, L. (2012) · Frontiers in Immunology · doi:10.3389/fimmu.2011.00096 · Cited by 127
“REVIEW ARTICLE published: 11 January 2012 doi: 10.3389/fimmu.2011.00096 Regulation of B cell functions by the sialic acid-binding receptors Siglec-G and CD22”
BackgroundMethodInfluentialThe role of HMGB1 in the pathogenesis of rheumatic disease
Andersson, U., & Harris, H. E. (2010) · Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms · doi:10.1016/j.bbagrm.2009.11.003 · Cited by 126
Roy, A., Ganesh, G., Sippola, H., Bolin, S., Sawesi, O., Dagälv, A., Schlenner, S., Feyerabend, T. B., Rodewald, H.-R., Kjellén, L., et al. (2013) · Journal of Biological Chemistry · doi:10.1074/jbc.m112.435156 · Cited by 132
Adaptive immunity after cell death
Zelenay, S., & Sousa, C. R. E. (2013) · Trends in Immunology · doi:10.1016/j.it.2013.03.005 · Cited by 129
Identification of CD163 as an antiinflammatory receptor for HMGB1-haptoglobin complexes
Yang, H., Wang, H., Levine, Y. A., Gunasekaran, M., Wang, Y., Addorisio, M. E., Zhu, S., Li, W., Li, J., de Kleijn, D. P. V., et al. (2016) · JCI Insight · doi:10.1172/jci.insight.85375 · Cited by 123
“Other plasma proteins that can bind HMGB1 and confer protection include thrombomodulin (38), soluble receptor for advanced glycation end products (s-RAGE) (39), and Siglec-10/CD24 (40).”
BackgroundSiglec receptors as new immune checkpoints in cancer
Stanczak, M. A., & Laubli, H. P. (2022) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2022.101112 · Cited by 127
Cetuximab-mediated Tumor Regression Depends on Innate and Adaptive Immune Responses
Yang, X., Zhang, X., Mortenson, E. D., Radkevich-Brown, O., Wang, Y., & Fu, Y. (2012) · Molecular Therapy · doi:10.1038/mt.2012.184 · Cited by 120
Bianchi, M. E., & Manfredi, A. A. (2009) · Science · doi:10.1126/science.1172794 · Cited by 117
Antigen Delivery to Macrophages Using Liposomal Nanoparticles Targeting Sialoadhesin/CD169
Chen, W. C., Kawasaki, N., Nycholat, C. M., Han, S., Pilotte, J., Crocker, P. R., & Paulson, J. C. (2012) · PLoS ONE · doi:10.1371/journal.pone.0039039 · Cited by 117
“The exception was moderate binding of 39-NeuAc liposomes to murine Siglec-G expressing cells, which is expressed on B cells, monocytes and dendritic cells (Figure 4B) [20–22].”
BackgroundLewis, D. H., Chan, D. L., Pinheiro, D., Armitage‐Chan, E. A., & Garden, O. A. (2012) · Journal of Veterinary Internal Medicine · doi:10.1111/j.1939-1676.2012.00905.x · Cited by 125
Role of siglecs and related glycan-binding proteins in immune responses and immunoregulation
Bochner, B. S., & Zimmermann, N. (2015) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2014.11.031 · Cited by 122
“Physiologic inhibitory signaling through Siglec-10 and Siglec-G occurs as a result of engagement of sialic acid residues on CD24, a glycosylphosphatidylinositol–linked protein on the surfaces of B cells and granulocytes.(90) In addition to CD24 as a ligand, some antigen-activated humanT cells suppress other T cells in…”
Laubli, H. P., Alisson‐Silva, F., Stanczak, M. A., Siddiqui, S. S., Deng, L., Verhagen, A., Varki, N. M., & Varki, A. P. (2014) · Journal of Biological Chemistry · doi:10.1074/jbc.m114.593129 · Cited by 117
“also recognize a rather broad spectrum of glycans with different protein backbones (12, 48-51).”
BackgroundTargeting the Siglec–Sialic Acid Immune Axis in Cancer: Current and Future Approaches
Laubli, H. P., Nalle, S. C., & Maslyar, D. J. (2022) · Cancer Immunology Research · doi:10.1158/2326-6066.cir-22-0366 · Cited by 117
“Siglec-10/G binding to a CD24 complex with high mobility group box 1 (HMGB1) has been shown to dampen the immune response to danger signals (55).”
BackgroundRomero, R. J., Chaiworapongsa, T., Savasan, Z. A., Hussein, Y., Dong, Z., Kusanovic, J. P., Kim, C. J., & Hassan, S. S. (2012) · The Journal of Maternal-Fetal & Neonatal Medicine · doi:10.3109/14767058.2011.599083 · Cited by 112
“Extracellular HMGB1 can potentially be associated with DNA, RNA, endotoxin, nucleosomes [24], thrombospondin [105–107] or CD24 [108,109] to augment or”
Nucleic acids and endosomal pattern recognition: how to tell friend from foe?
Brencicova, E., & Diebold, S. S. (2013) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2013.00037 · Cited by 118
Siglec Signaling in the Tumor Microenvironment
van Houtum, E. J. H., Büll, C., Cornelissen, L. A. M., & Adema, G. J. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.790317 · Cited by 111
“CD24 and CD52 have been shown to complex with HMGB1, adding even an additional layer of complexity, as binding of Siglec-10 to CD52 has even been shown to be enhanced by HGMB1 (95, 103, 104).”
BackgroundSiglecs as sensors of self in innate and adaptive immune responses
Paulson, J. C., Macauley, M. S., & Kawasaki, N. (2012) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2011.06362.x · Cited by 113
Putting the brakes on phagocytosis: “don't-eat-me” signaling in physiology and disease
Kelley, S. M., & Ravichandran, K. S. (2021) · EMBO Reports · doi:10.15252/embr.202152564 · Cited by 117
“Signaling through this axis suppresses NF-j B-mediated inflammation in response to damage-associated molecular patterns via SHP-1 activation (Chen et al, 2009; Chen et al, 2011).”
InfluentialBoligan, K. F., Mesa, C., Fernandez, L. E., & von Gunten, S. (2014) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-014-1799-5 · Cited by 110
“It has been proposed that by their capacity to discriminate between PAMP and ‘SAMP’ or DAMP, siglecs may play a role in the protection of self tissue as well as the repression of tissue damage-induced immune responses [16, 121].”
Trained immunity in organ transplantation
Ochando, J., Fayad, Z. A., Madsen, J. C., Netea, M. G., & Mulder, W. J. M. (2019) · American Journal of Transplantation · doi:10.1111/ajt.15620 · Cited by 113
“39 Thus, molecules that activate danger signaling pathways that trigger im‐ mune responses may also participate in the negative regulation of TLR responses as a control for excessive inflammation.”
Ding, Y., Guo, Z., Liu, Y., Li, X., Zhang, Q., Xu, X., Gu, Y., Zhang, Y., Zhao, D., & Cao, X. (2016) · Nature Immunology · doi:10.1038/ni.3535 · Cited by 110
Self-citationRauvala, H., & Rouhiainen, A. (2009) · Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms · doi:10.1016/j.bbagrm.2009.11.012 · Cited by 106
Doyle, T. J., Kaur, G., Putrevu, S. M., Dyson, E. L., Dyson, M. T., McCunniff, W. T., Pasham, M. R., Kim, K. H., & Dufour, J. M. (2011) · Biology of Reproduction · doi:10.1095/biolreprod.110.089425 · Cited by 109
“CD24 (alias, heat-stable antigen [HSA]) enhanced the intercellular barrier function of tight junctional proteins and decreased immune response following acute tissue damage [39, 40].”
BackgroundSpermine protects mice against lethal sepsis partly by attenuating surrogate inflammatory markers
Zhu, S., Ashok, M., Li, J., Li, W., Yang, H., Wang, P., Tracey, K. J., Sama, A. E., & Wang, H. (2009) · Molecular Medicine · doi:10.2119/molmed.2009.00062 · Cited by 109
“These experimental results were consistent with recent findings that highly purified HMGB1 induces much less TNF and IL-6 than those induced by LPS in macrophage/monocytes (38) and dendritic cells (9).”
Cancer immunogenicity, danger signals, and DAMPs: What, when, and how?
Garg, A. D., Dudek, A. M., & Agostinis, P. (2013) · BioFactors · doi:10.1002/biof.1125 · Cited by 116
“In fact, DAMPs (like HMGB1, HSP70, and HSP90) but not PAMPs (like LPS) engage the CD24-Siglec G/10 surface protein complex on immune cells, which subsequently suppresses immune response as reflected by the decrease in NF-kB activation [56].”
BackgroundArmed response: how dying cells influence T‐cell functions
Ferguson, T. A., Choi, J., & Green, D. R. (2011) · Immunological Reviews · doi:10.1111/j.1600-065x.2011.01006.x · Cited by 118
“Perhaps we were unable to detect HMGB1 effects because we simply did not use enough of the protein; however, a recent paper (94) examining the role of CD24 in the regulation of HMGB1 function found little cytokine production from DCs in the absence of this cell surface protein.”
High‐Mobility Group Box‐1 and Liver Disease
Gaskell, H., Ge, X., & Nieto, N. (2018) · Hepatology Communications · doi:10.1002/hep4.1223 · Cited by 104
“HMGB1 binds multiple receptors, including RAGE, toll-like receptors (TLRs) 2/4/9, Mac-1, syndecan-1, phosphacan protein-tyrosine phosphatase-ζ/β, and clusters of differentiation 24.(11,90‒93) Due to the dominant role of RAGE and TLR4 in liver disease, we focus on these two receptors.”
BackgroundMolecular Mechanism of Tumor Cell Immune Escape Mediated by CD24/Siglec-10
Yin, S.-S., & Gao, F. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.01324 · Cited by 107
“Siglec-10 binds firmly to CD24 in a sialylation-dependent manner, and CD24 is the main ligand of Siglec-10 (41, 42).”
BackgroundInfluentialFong, J. J., Sreedhara, K., Deng, L., Varki, N. M., Angata, T., Liu, Q., Nizet, V., & Varki, A. P. (2015) · The EMBO Journal · doi:10.15252/embj.201591407 · Cited by 104
“Examples include the well-studied high mobility group box 1 protein (HMGB1) (Wang et al , 1999; Chen et al , 2009) and the less well-explored Hsp70 (Asea et al , 2000).”
High-mobility group box-1 and its role in angiogenesis
Yang, S., Xu, L., Yang, T., & Wang, F. (2014) · Journal of Leukocyte Biology · doi:10.1189/jlb.0713412 · Cited by 104
“As a secreted protein, HMGB1 serves its proinflammatory function through RAGE, TLR2, TLR4, TLR9, Mac-1, CXCR4, CXCR12, TIM-3, and CD24-Siglec-10 (Siglec-G in mice) and activates a series of signaling pathways, including MAPKs, PI3K/Akt, and NF- B, all of which play significant roles in inflammation and angiogenesis (T…”
BackgroundHigh Mobility Group Box-1 (HMGb1): Current Wisdom and Advancement as a Potential Drug Target
VanPatten, S., & Al‐Abed, Y. (2017) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.7b01136 · Cited by 103
Chen, C., Liu, Y., Liu, Y., & Zheng, P. (2010) · Journal of Clinical Investigation · doi:10.1172/jci43873 · Cited by 105
Self-citationHigh-mobility group box 1 (HMGB1) as a master regulator of innate immunity
Castiglioni, A., Canti, V., Rovere, P. Q., & Manfredi, A. A. (2010) · Cell and Tissue Research · doi:10.1007/s00441-010-1033-1 · Cited by 104
Endogenous IL-10 Attenuates Cisplatin Nephrotoxicity: Role of Dendritic Cells
Tadagavadi, R. K., & Reeves, W. B. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.1000383 · Cited by 107
“crotic cells produce proinflammatory cytokines (54).”
Regulation of immunological and inflammatory functions by biotin
Kuroishi, T. (2015) · Canadian Journal of Physiology and Pharmacology · doi:10.1139/cjpp-2014-0460 · Cited by 100
“CD24 was previously reported to be a receptor 22 for HSPs, and the HSPs-CD24 axis negatively regulated immunological and 23 inflammatory responses (Chen et al. 2009).”
Zhang, C., Feng, J., Du, J., Zhuo, Z., Yang, S., Zhang, W., Wang, W., Zhang, S., Iwakura, Y., Meng, G., et al. (2018) · Cellular & Molecular Immunology · doi:10.1038/cmi.2017.22 · Cited by 99
TLR4-dependent activation of dendritic cells by an HMGB1-derived peptide adjuvant
Saenz, R., Futalan, D., Leutenez, L., Eekhout, F., Fecteau, J. F., Sundelius, S., Sundqvist, S., Larsson, M., Hayashi, T., Minev, B., et al. (2014) · Journal of Translational Medicine · doi:10.1186/1479-5876-12-211 · Cited by 100
“Several receptors have been implicated, including RAGE, TLR4, TLR2, CD24/Siglec-10.”
BackgroundDendritic Cells: A Spot on Sialic Acid
Crespo, H. J., Lau, J. T. Y., & Videira, P. A. (2013) · Frontiers in Immunology · doi:10.3389/fimmu.2013.00491 · Cited by 98
“Chen and co-workers reported Siglec-10 as involved in helping distinguish TLR-recognized danger-associated molecular patterns (DAMPs) – generated during cell/tissue damage or even regular cell lifecycle – from PAMPs, thus controlling inflammation (100).”
BackgroundDickel, H., Gambichler, T., Kamphowe, J., Altmeyer, P. J., & Skrygan, M. (2010) · Contact Dermatitis · doi:10.1111/j.1600-0536.2010.01769.x · Cited by 98
“Both heat shock proteins have been only recently classified as ‘alarmins’ (17, 24, 25), a subgroup of the damageassociated molecular pattern family (26).”
BackgroundThe role of dendritic cells in the pathogenesis of systemic lupus erythematosus
Fransen, J. H., van der Vlag, J., Ruben, J. M., Adema, G. J., Berden, J. H. M., & Hilbrands, L. B. (2010) · Arthritis Research & Therapy · doi:10.1186/ar2966 · Cited by 97
The Danger Signal S100B Integrates Pathogen– and Danger–Sensing Pathways to Restrain Inflammation
Sorci, G., Giovannini, G., Riuzzi, F., Bonifazi, P., Zelante, T., Zagarella, S., Bistoni, F., Donato, R., & Romani, L. R. (2011) · PLoS Pathogens · doi:10.1371/journal.ppat.1001315 · Cited by 100
“Supporting Information Figure S1 RAGE and DAMPs expression in pulmonary aspergillosis.”
BackgroundInfluentialExtracellular High-Mobility Group Box 1 Protein (HMGB1) as a Mediator of Persistent Pain
Agalave, N. M., & Svensson, C. I. (2014) · Molecular Medicine · doi:10.2119/molmed.2014.00176 · Cited by 99
Emerging role of HMGB1 in lung diseases: friend or foe
Ding, J., Cui, X., & Liu, Q. (2016) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.13048 · Cited by 95
“Among these receptors, TIM-3 and CD24 act as negative receptors and inhibit immune activity of HMGB1 in tumour-associated dendritic cells (TADCs) and macrophages, respectively [50, 51].”
BackgroundDanger Signals and Graft-versus-host Disease: Current Understanding and Future Perspectives
Toubai, T., Mathewson, N. D., Magenau, J. M., & Reddy, P. R. (2016) · Frontiers in Immunology · doi:10.3389/fimmu.2016.00539 · Cited by 96
“for DAMPs-Mediated inflammation Sialic acid-binding immunoglobulin like lectins (Siglecs) have an immunoreceptor tyrosine-based inhibitory motifs (ITIM) or ITIM-like regions in their intracellular domains and negatively regulate DAMPs-mediated innate inflammatory responses (177, 178) or induce B-cell tolerance by supp…”
BackgroundCD33‐related siglecs as potential modulators of inflammatory responses
Crocker, P. R., McMillan, S. J., & Richards, H. E. (2012) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2011.06449.x · Cited by 95
Siglec-G–CD24 axis controls the severity of graft-versus-host disease in mice
Toubai, T., Hou, G., Mathewson, N. D., Liu, C., Wang, Y., Oravecz-Wilson, K. I., Cummings, E. L., Rossi, C., Evers, R., Sun, Y., et al. (2014) · Blood · doi:10.1182/blood-2013-12-545335 · Cited by 94
“CD24 is also the high-affinity ligand for Siglec-G.(4) CD24 is associated with a broad range of DAMPs, such as via HSP70, HSP90, and HMGB-1, binds to Siglec-G and then represses the responses to these DAMPs via the activation of ITIMs.”
BackgroundResultInfluentialSelf-citationImmune inhibitory receptors: Essential regulators of phagocyte function
Steevels, T. A. M., & Meyaard, L. (2011) · European Journal of Immunology · doi:10.1002/eji.201041179 · Cited by 92
Ratliff, B. B., Rabadi, M. M., Vasko, R., Yasuda, K., & Goligorsky, M. S. (2013) · Journal of the American Society of Nephrology · doi:10.1681/asn.2012060633 · Cited by 99
Host and pathogen hyaluronan signal through human siglec-9 to suppress neutrophil activation
Secundino, I., Lizcano, A., Roupé, K. M., Wang, X., Cole, J. N., Olson, J., Ali, S. R., Dahesh, S., Amayreh, L. K., Henningham, A., et al. (2016) · Journal of Molecular Medicine · doi:10.1007/s00109-015-1341-8 · Cited by 92
“If regulation by inhibitory CD33rSiglecs is perturbed, pathologies may ensue including eosinophilic airway inflammation in mSiglec-F knockout mice [14], elevated proinflammatory cytokines in mice lacking mSiglec-G [8], asthma associated with hSiglec-8 polymorphisms [15], or exaggerated T cell responses linked to an hS…”
BackgroundBandala‐Sanchez, E., Bediaga, N. G., Goddard‐Borger, E. D., Ngui, K., Naselli, G., Stone, N. L., Neale, A. M., Pearce, L. A., Wardak, A. Z., Czabotar, P. E., et al. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1722056115 · Cited by 91
“Another GPI-anchored protein, CD24, with a gene organization structure resembling that of CD52 (12), was reported to bind Siglec-10 by first associating with damage-associated molecular pattern (DAMP) proteins, including high mobility group box 1 (HMGB1) (13).”
BackgroundHMGB1 and repair: focus on the heart
Pellegrini, L., Foglio, E., Pontemezzo, E., Germani, A., Russo, M. A., & Limana, F. (2018) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2018.12.005 · Cited by 92
Kruse, K., Janko, C., Urbonaviciute, V., Mierke, C. T., Winkler, T., Voll, R. E., Schett, G. A., Munoz, L. E., & i, M. H. (2010) · APOPTOSIS · doi:10.1007/s10495-010-0478-8 · Cited by 94
Siglec-G/10 in self-nonself discrimination of innate and adaptive immunity
Chen, G.-Y., Brown, N. K., Zheng, P., & Liu, Y. (2014) · Glycobiology · doi:10.1093/glycob/cwu068 · Cited by 90
“The negative regulation is reflected at the level of DCs, as Cd24−/− and Siglecg−/− DC exhibit significantly enhanced responses to HMGB1 (Chen et al. 2009).”
BackgroundInfluentialSelf-citationResolution-associated molecular patterns (RAMP): RAMParts defending immunological homeostasis?
Shields, A. M., Panayi, G. S., & Corrigall, V. M. (2011) · Clinical and Experimental Immunology · doi:10.1111/j.1365-2249.2011.04433.x · Cited by 90
Advances in understanding the pathogenesis of graft‐versus‐host disease
Magenau, J. M., Runaas, L., & Reddy, P. R. (2016) · British Journal of Haematology · doi:10.1111/bjh.13959 · Cited by 90
“Under conditions of immune activation of DCs via PAMPs (e.g. lipopolysaccharide) or stimulation of T cells by allogeneic DCs, the differential overexpression of the haematopoieticspecific miR, miR-142 (MIR142), was substantially greater than other miRs.”
BackgroundInfluentialCD24: A Novel Target for Cancer Immunotherapy
Panagiotou, Ε., Syrigos, N. K., Charpidou, A. G., Kotteas, E. A., & Vathiotis, I. A. (2022) · Journal of Personalized Medicine · doi:10.3390/jpm12081235 · Cited by 93
“sion of the immune response following tissue damage [70,71].”
BackgroundCD24 Overexpression Is Associated with Poor Prognosis in Luminal A and Triple-Negative Breast Cancer
Kwon, M. J., Han, J., Seo, J., Song, K., Jeong, H. M., Choi, J., Kim, Y. J., Lee, S. H., Choi, Y., & Shin, Y. K. (2015) · PLoS ONE · doi:10.1371/journal.pone.0139112 · Cited by 90
“However, a recent study revealed that CD24 suppresses the immune response through interaction with Siglec protein expressed on immune cells [33], and this may suggest the possible contribution of CD24-Siglec pathway to the cancer immune escape.”
BackgroundAbdulmahdi, W., Patel, D., Rabadi, M. M., Azar, T., Jules, E., Lipphardt, M., Hashemiyoon, R., & Ratliff, B. B. (2017) · Redox Biology · doi:10.1016/j.redox.2017.08.001 · Cited by 90
HMGB1 in renal ischemic injury
Rabadi, M. M., Ghaly, T., Goligorksy, M. S., & Ratliff, B. B. (2012) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00092.2012 · Cited by 91
Rai, V., Wood, M. B., Feng, H., Schabla, N. M., Tu, S., & Zuo, J. (2020) · Scientific Reports · doi:10.1038/s41598-020-72181-6 · Cited by 88
Targeting Siglecs—A novel pharmacological strategy for immuno- and glycotherapy
Jandus, C., Simon, H., & von Gunten, S. (2011) · Biochemical Pharmacology · doi:10.1016/j.bcp.2011.05.018 · Cited by 88
Sialic acids and autoimmune disease
Mahajan, V. S., & Pillai, S. S. (2015) · Immunological Reviews · doi:10.1111/imr.12344 · Cited by 88
“Mice that lack CD24 or Siglec-G are susceptible to a sublethal challenge of acetaminophen and die from a severe liver injury within 20 h of acetaminophen administration (107).”
BackgroundCellular and molecular choreography of neutrophil recruitment to sites of sterile inflammation
McDonald, B., & Kubes, P. (2011) · Journal of Molecular Medicine · doi:10.1007/s00109-011-0784-9 · Cited by 93
“Furthermore, there is evidence that infection and tissue injury can be differentiated at the level of danger signal recognition [ 85 ].”
BackgroundEscamilla-Tilch, M., Filio‐Rodríguez, G., García‐Rocha, R., Mancilla‐Herrera, I., Mitchison, N. A., Ruiz‐Pacheco, J. A., Sánchez‐García, F. J., Sandoval‐Borrego, D., & Vázquez-Sánchez, E. A. (2013) · Immunology and Cell Biology · doi:10.1038/icb.2013.58 · Cited by 87
Stephenson, H. N., Mills, D. C., Jones, H. E., Enea, M., Copland, A., Dorrell, N., Wren, B. W., Crocker, P. R., Escors, D., & Bajaj‐Elliott, M. (2014) · The Journal of Infectious Diseases · doi:10.1093/infdis/jiu287 · Cited by 85
“mediated signalling [17, 18].”
Copresentation of Antigen and Ligands of Siglec-G Induces B Cell Tolerance Independent of CD22
Pfrengle, F., Macauley, M. S., Kawasaki, N., & Paulson, J. C. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1300921 · Cited by 84
“In addition to its function in B cells, Siglec-G has also been shown to play an important role in dendritic cells by discriminating dangerassociated molecular patterns from pathogen-associated molecular patterns (PAMPs) (13).”
BackgroundUrbonaviciute, V., & Voll, R. E. (2011) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2011.02432.x · Cited by 85
Kato, J., & Svensson, C. I. (2015) · Progress in molecular biology and translational science · doi:10.1016/bs.pmbts.2014.11.014 · Cited by 85
HMGB1 blockade attenuates experimental autoimmune myocarditis and suppresses Th17‐cell expansion
Su, Z., Sun, C., Zhou, C., Liu, Y., Zhu, H., Sandoghchian, S., Zheng, D., Peng, T., Zhang, Y., Jiao, Z., et al. (2011) · European Journal of Immunology · doi:10.1002/eji.201141879 · Cited by 81
Self-citationSu, Z., Zhang, P., Yu, Y., Lu, H., Liu, Y., Ni, P., Su, X., Wang, D., Liu, Y., Wang, J., et al. (2016) · Scientific Reports · doi:10.1038/srep21884 · Cited by 83
Self-citationRetractedGe, Y., Huang, M., & Yao, Y.-M. (2021) · Cells · doi:10.3390/cells10051044 · Cited by 86
“Binding of HMGB1 to CD24/Siglec-10 receptor suppresses HMGB1-mediated NF-κB signaling and following release of pro-inflammatory molecules [76].”
BackgroundMacrophages as a “weapon” in anticancer cellular immunotherapy
Aminin, D. L., & Wang, Y. (2021) · The Kaohsiung Journal of Medical Sciences · doi:10.1002/kjm2.12405 · Cited by 82
Synthetic Siglec-9 Agonists Inhibit Neutrophil Activation Associated with COVID-19
Delaveris, C. S., Wilk, A. J., Riley, N. M., Stark, J. C., Yang, S. S., Rogers, A. J., Ranganath, T., Nadeau, K. C., Biobank, T. S. C.-1., Blish, C. A., et al. (2021) · ACS Central Science · doi:10.1021/acscentsci.0c01669 · Cited by 82
Discovery, classification, evolution and diversity of Siglecs
Angata, T., & Varki, A. P. (2022) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2022.101117 · Cited by 77
Inflammation Aggravates Disease Severity in Marfan Syndrome Patients
Radonic, T., Witte, P. D., Groenink, M., de Waard, V., Lutter, R., van Eijk, M., Jansen, M., Timmermans, J., Kempers, M., Scholte, A., et al. (2012) · PLoS ONE · doi:10.1371/journal.pone.0032963 · Cited by 81
“CD24 is known to selectively repress tissue damage-induced immune responses [17] and in that light high CD24 is anti-inflammatory.”
BackgroundCanelli, E., Catella, A., Borghetti, P., Ferrari, L., Ogno, G., Angelis, E. D., Corradi, A., Passeri, B., Bertani, V., Sandri, G., et al. (2017) · Veterinary Microbiology · doi:10.1016/j.vetmic.2017.09.002 · Cited by 78
“Moreover, the relationship between NSP2 variation and biological properties such as PRRSV virulence, pathogenicity, tissue tropism and cell invasion ability has also been the subject of recent study (Chen et al., 2009; Wang and Zhang, 2014; Wang et al., 2013).”
Background
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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