Toll-like receptor 9–dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE

By Jane Tian, A. Avalos, S. Mao, Bo Chen, K. Senthil, Herren Wu, P. Parroche, Stacey Drabic, D. Golenbock, C. Sirois and 12 more. Nature Immunology, 2007

1,446 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Immunology

View Paper: https://www.semanticscholar.org/paper/b7adcd6b4eb109c85c2c04d2e04c5937062f10c9

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In Clinical Biochemistry

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

In Immunology

1. T. Mogensen
2. Shizuo Akira
3. O. Takeuchi
4. L. Galluzzi
5. Guido Kroemer
6. Kevin J. Tracey
7. Michael Lotze
8. D. Tang

Citations in the corpus

• HMGB1 Is a Therapeutic Target for Sterile Inflammation and Infection (2011, background): “B lymphocytes Nuclear assistance in VDJ recombination; potentiated activation by HMGB1-DNA-IgG complexes (129, 130)”
• PAMPs and DAMPs: Signal 0s that Spur Autophagy and Immunity (2012, background): “In addition, interaction between RAGE and TLR9 contributes to autoimmune pathogenesis (77), whereas interaction between RAGE and TLR2 limits inflammation (201).”
• Netting Neutrophils Are Major Inducers of Type I IFN Production in Pediatric Systemic Lupus Erythematosus (2011, background): “Furthermore, anti-RNP antibodies induce SLE but not healthy neutrophils to secrete high levels of LL37 and HMGB1, two endogenous proteins that contribute to increase the immunogenicity and uptake of mammalian DNA by pDCs (38, 24).”
• HMGB1: Endogenous Danger Signaling (2008, background): “who demonstrated that HMGB1-DNA complexes activate TLR9 signaling (64).”
• Mechanisms of diabetic complications. (2013, background): “However, the intrinsic role of RAGE in innate and adaptive immunity (366, 405, 599) must be considered carefully during the design of potential pharmacological agents to treat complications in the already potentially immunocompromised environment of diabetes.”
• Macrophage activation by endogenous danger signals (2008, background): “The resultant complex induced association of TLR9 and RAGE to activate plasmacytoid DCs to produce IFNα.”
• Decoding cell death signals in liver inflammation. (2013, background): “The circulating levels of mitochondrial DNA and N-formyl peptides, both of which are reminiscent of the endosymbiotic origin of these organelles, are elevated in patients undergoing acute liver failure Journal of Hepatology 201 [152].”