CD24 and Siglec-10 Selectively Repress Tissue Damage–Induced Immune Responses

By Guo-Yun Chen, Jie Tang, P. Zheng, Yang Liu. Science, 2009

774 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/fc7f04c13e1e65ff51a2011a1a218c0ed18246f8

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Clinical Biochemistry

1. D. Tang
2. R. Kang
3. H. J. Zeh
4. Michael Lotze
5. Kevin J. Tracey
6. U. Andersson
7. A. Piccinini
8. K. Midwood

In Immunology

1. L. Galluzzi
2. Guido Kroemer
3. H. J. Zeh
4. Oliver Kepp
5. D. Tang
6. R. Kang
7. Michael Lotze
8. Kevin J. Tracey

In Molecular Biology

1. Guido Kroemer
2. D. Tang
3. R. Kang
4. L. Galluzzi
5. Oliver Kepp
6. C. Brenner
7. H. J. Zeh
8. Michael Lotze

Citations in the corpus

• HMGB1 Is a Therapeutic Target for Sterile Inflammation and Infection (2011, positive): “by immunocytes, which in turn associates with Siglec-10 to selectively suppress the nuclear translocation of NF-κB induced by HMGB1-mediated TLR4 activation, but not pathogen-mediated TLR activation (29).”
• Tumour-initiating cells: challenges and opportunities for anticancer drug discovery (2009, background): “Certain markers used for prospective sorting may also select for cells that evade the immune syste”
• PAMPs and DAMPs: Signal 0s that Spur Autophagy and Immunity (2012, background): “CD24 serves as a negative signaling molecule to limit DAMP- but not PAMP-mediated inflammation (73).”
• Phagocyte partnership during the onset and resolution of inflammation (2010, background): “Interestingly, it has recently been shown that HMGB1 can interact with CD24 , a glycosylphosphatidylinositol (GPI)-anchored membrane protein, which in turn binds sialic acid-binding immunoglobulin-like lectin G (SIGLECG”
• Immune activation in brain aging and neurodegeneration: too much or too little? (2009, background): “Additional receptors also exist that appear to selectively recognize DAMPs, including CD24 and receptor for advanced glycation end-products (RAGE) (Arancio et al., 2004; Chen et al., 2009).”
• Decoding cell death signals in liver inflammation. (2013, background): “HSPs Molecular chaperons Adjuvants Anti-inflammatory function (?) TLR2 TLR4 Released upon PMP or secreted via active, exosome-dependent routes Implicated in the response to hepatic IR and other hepatotoxic conditions [48, 134-136]”
• DAMPening Inflammation by Modulating TLR Signalling (2010, background): “Dysfunction of this pathway might contribute to the etiology of autoimmune diseases and likewise may offer a means to selectively inhibit DAMP activity [198].”
• Biological roles of glycans (2016, background): “A clear example of glycan-based SAMPs has been reported in the form of inhibitory Siglec recognition of cell surface sialoglycans (962) (963) (964) , which may also provide a mechanism for the host to discriminate between infectious nonself and noninfectious self (965) .”