The Immune Tolerance Role of the HMGB1-RAGE Axis

The disruption of the immune tolerance induces autoimmunity such as systemic lupus erythematosus and vasculitis. A chromatin-binding non-histone protein, high mobility group box 1 (HMGB1), is released from the nucleus to the extracellular milieu in particular environments such as autoimmunity, sepsi...

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Autores principales: Watanabe, Haruki, Son, Myoungsun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8001022/
https://www.ncbi.nlm.nih.gov/pubmed/33807604
http://dx.doi.org/10.3390/cells10030564
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author Watanabe, Haruki
Son, Myoungsun
author_facet Watanabe, Haruki
Son, Myoungsun
author_sort Watanabe, Haruki
collection PubMed
description The disruption of the immune tolerance induces autoimmunity such as systemic lupus erythematosus and vasculitis. A chromatin-binding non-histone protein, high mobility group box 1 (HMGB1), is released from the nucleus to the extracellular milieu in particular environments such as autoimmunity, sepsis and hypoxia. Extracellular HMGB1 engages pattern recognition receptors, including Toll-like receptors (TLRs) and the receptor for advanced glycation endproducts (RAGE). While the HMGB1-RAGE axis drives inflammation in various diseases, recent studies also focus on the anti-inflammatory effects of HMGB1 and RAGE. This review discusses current perspectives on HMGB1 and RAGE’s roles in controlling inflammation and immune tolerance. We also suggest how RAGE heterodimers responding microenvironments functions in immune responses.
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spelling pubmed-80010222021-03-28 The Immune Tolerance Role of the HMGB1-RAGE Axis Watanabe, Haruki Son, Myoungsun Cells Review The disruption of the immune tolerance induces autoimmunity such as systemic lupus erythematosus and vasculitis. A chromatin-binding non-histone protein, high mobility group box 1 (HMGB1), is released from the nucleus to the extracellular milieu in particular environments such as autoimmunity, sepsis and hypoxia. Extracellular HMGB1 engages pattern recognition receptors, including Toll-like receptors (TLRs) and the receptor for advanced glycation endproducts (RAGE). While the HMGB1-RAGE axis drives inflammation in various diseases, recent studies also focus on the anti-inflammatory effects of HMGB1 and RAGE. This review discusses current perspectives on HMGB1 and RAGE’s roles in controlling inflammation and immune tolerance. We also suggest how RAGE heterodimers responding microenvironments functions in immune responses. MDPI 2021-03-05 /pmc/articles/PMC8001022/ /pubmed/33807604 http://dx.doi.org/10.3390/cells10030564 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ).
spellingShingle Review
Watanabe, Haruki
Son, Myoungsun
The Immune Tolerance Role of the HMGB1-RAGE Axis
title The Immune Tolerance Role of the HMGB1-RAGE Axis
title_full The Immune Tolerance Role of the HMGB1-RAGE Axis
title_fullStr The Immune Tolerance Role of the HMGB1-RAGE Axis
title_full_unstemmed The Immune Tolerance Role of the HMGB1-RAGE Axis
title_short The Immune Tolerance Role of the HMGB1-RAGE Axis
title_sort immune tolerance role of the hmgb1-rage axis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8001022/
https://www.ncbi.nlm.nih.gov/pubmed/33807604
http://dx.doi.org/10.3390/cells10030564
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