HMGB1 is a therapeutic target for sterile inflammation and infection
Open accessAbstract
A key question in immunology concerns how sterile injury activates innate immunity to mediate damaging inflammation in the absence of foreign invaders. The discovery that HMGB1, a ubiquitous nuclear protein, mediates the activation of innate immune responses led directly to the understanding that HMGB1 plays a critical role at the intersection of the host inflammatory response to sterile and infectious threat. HMGB1 is actively released by stimulation of the innate immune system with exogenous pathogen-derived molecules and is passively released by ischemia or cell injury in the absence of invasion. Established molecular mechanisms of HMGB1 binding and signaling through TLR4 reveal signaling pathways that mediate cytokine release and tissue damage. Experimental strategies that selectively target HMGB1 and TLR4 effectively reverse and prevent activation of innate immunity and significantly attenuate damage in diverse models of sterile and infection-induced threat.
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HMGB1 is a major pro-inflammatory SASP factor when externalized from the nucleus into the extracellular environment.
“The non-histone DNA-binding protein high mobility group protein B1 (HMGB1) is a major pro-inflammatory SASP factor, when externalized from the nucleus into the extracellular environment.39”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [39]
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Immunogenic Cell Death in Cancer Therapy
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Mutually exclusive redox forms of HMGB1 promote cell recruitment or proinflammatory cytokine release
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“Notably, immune cells secrete HMGB1 when activated by infection or tissue damage (Andersson and Tracey, 2011); mesothelioma and other cancer cells secrete HMGB1 constitutively (Jube et al., 2012).”
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Self-citationSterile inflammation in the liver
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- Authors
- Andersson, U., & Tracey, K. J.
- Affiliations
- Karolinska University Hospital (SE)
- Feinstein Institute for Medical Research (US)
- ORCID
- Tracey, Kevin J.
- Venue
- Annual Review of Immunology
- Publisher
- Annual Reviews
- Published
- 2011-04-23
- Volume
- 29
- Issue
- 1
- Pages
- 139-162
- ISSN
- 0732-0582 (ISSN-L)
- 1545-3278
- PMC
- PMC4536551
- OpenAlex
- W2114445825
- Cited by
- 1,437
- References
- 148
- Citations by year
- 2026: 76 · 2025: 70 · 2024: 74 · 2023: 69 · 2022: 100 · 2021: 126 · 2020: 94 · 2019: 95 · 2018: 105 · 2017: 89 · 2016: 106 · 2015: 100 · 2014: 131 · 2013: 94 · 2012: 76
- FWCI
- 12.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annual Review of Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM062508)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- HMGB1, sterile inflammation, infection, innate immunity, TLR4, HMGB1 release, HMGB1 signaling, cytokine production, tissue damage, ischemia, cell damage
- MeSH terms
- Animals, Humans, Immunity, Innate, Infections, Inflammation, Drug Delivery Systems, HMGB1 Protein, Toll-Like Receptor 4
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