Reversing established sepsis with antagonists of endogenous high-mobility group box 1

By Huan Yang, M. Ochani, Jianhua Li, X. Qiang, Mahira Tanović, H. Harris, Srinivas M Susarla, Luis Ulloa, Hong Wang, R. DiRaimo and 8 more. Proceedings of the National Academy of Sciences of the United States of America, 2003

1,186 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/6802f18f25cf839b67e6edd5d2b0c3a3836fe460

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

In Immunology

In Molecular Biology

Citations in the corpus

A critical cysteine is required for HMGB1 binding to Toll-like receptor 4 and activation of macrophage cytokine release (2010, methodology): “coli and purified to homogeneity as previously described (3, 16, 24).”
High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal (2005, methodology): “In a standardized model in which mice are administered lipopolysaccharide (LPS) to generate endotoxaemia, serum HMGB1 levels begin to increase 12–18 hours after peak levels of TNF, which occur at 2 hours, and of IL-1, which occur at 4–6 hour”
The nuclear factor HMGB1 mediates hepatic injury after murine liver ischemia-reperfusion (2005, background): “High-mobility group box 1 (HMGB1) recently was identified as an inflammatory cytokine that is involved as a late mediator of lethality in sepsis (9, 10).”
HMGB1: Endogenous Danger Signaling (2008, background): “In comparison, the A-box does not possess the pro-inflammatory properties of the B-box and instead competes with HMGB1 for binding sites leading to attenuation of the inflammatory cascade (24).”
DAMPs, PAMPs and alarmins: all we need to know about danger (2007, background): “Extranuclear expression of HMGB1 has been involved in a number of pathogenic conditions: sepsis [44], arthritis [45, 46], atherosclerosis [10], systemic lupus erythematosus (SLE) [47], cancer [48] and hepatitis [49, this issue].”
DAMPening Inflammation by Modulating TLR Signalling (2010, background): “Administration of polyclonal anti-HMGB1 antibodies or the DNA-binding A box of HMGB1, a competitive inhibitor of the pro-inflammatory B box, can reverse the lethality of established sepsis [114, 153, 154] and ameliorate collageninduced arthritis in rodents (reviewed in [161]).”
The role of oxidative stress during inflammatory processes (2013, background): “Received August 19, 2013; accepted October 9, 2013; previously published online October 10, 2013”
High mobility group box 1 protein interacts with multiple Toll-like receptors. (2006, background): “Although the participation of multiple receptors in HMGB1 signaling is somewhat surprising, similar results have been reported by other investigators, who also found that HMGB1 could activate cells through TLR-dependent and -independent pathways (43, 46).”
Sepsis: current dogma and new perspectives. (2014, background): “…specific, neutralizing monoclonal antibodies or by pharmacological agents that suppress serum HMGB1 concentrations confers survival advantages to animals with severe sepsis and protects against impaired organ function and homeostasis (Qin et al., 2006; Ulloa et al., 2002; Yang et al., 2004, 2011).”