Mutually exclusive redox forms of HMGB1 promote cell recruitment or proinflammatory cytokine release

By E. Vénéreau, Maura Casalgrandi, M. Schiraldi, D. Antoine, A. Cattaneo, F. De Marchis, J. Liu, A. Antonelli, A. Preti, L. Raeli and 8 more. Journal of Experimental Medicine, 2012

726 citations recorded by the source corpus.

HMGB1 orchestrates leukocyte recruitment and their induction to secrete inflammatory cytokines by switching between mutually exclusive redox states.

Subfields: Clinical Biochemistry, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/17d0978fd742005f41f9a10b50083eec9ce6ff3d

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Citations in the corpus

Immunogenic cell death and DAMPs in cancer therapy (2012, background): “These authors showed that a recombinant N-terminal fragment of CRT (39-272) is a potent inducer of activation and maturation of B cells and macrophages and can trigger Ig class switching in B cells without T cell help in vitro and in vivo72.”
Vascular Inflammation and Oxidative Stress: Major Triggers for Cardiovascular Disease (2019, background): “Reduction of all thiols in HMGB1 makes it a chemokine, a disulfide bond between Cys23 and Cys45 converts it to a proinflammatory cytokine, and oxidation of all thiols makes it inactive [215].”
The role of oxidative stress during inflammatory processes (2013, background): “These two distinct redox forms of HMGB1 are mutually exclusive, which implies that, depending on the particular microenvironment, HMGB1 functions either as a chemo attractant or as an inducer of cytokine release (Tang et al., 2012a; Venereau et al., 2012).”
Oxidant Mechanisms in Renal Injury and Disease (2016, neutral): “However, as these cysteine residues become oxidized to disulfide bonds, the reparative effects of the protein are loss, and instead HMGB1 promotes inflammation and damage (307,330).”
Sepsis: current dogma and new perspectives. (2014, background): “There are three HMGB1 isoforms, termed disulfide HMGB1, fully reduced HMGB1, and sulfonyl HMGB1, and each signal through mutually exclusive HMGB1 receptor superfamily members expressed on endothelial and epithelial cells (Antoine et al., 2014; Venereau et al., 2012; Yang et al., 2012).”
Nanomedicine-Driven Modulation of the Gut–Brain Axis: Innovative Approaches to Managing Chronic Inflammation in Alzheimer’s and Parkinson’s Disease (2025, unknown): “The disulfide form, in particular, is associated with cytokine-inducing potential and is elevated in CSF of patients with AD and PD [26].”