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REVIEW article

Front. Immunol.

Sec. Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders

Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1569632

This article is part of the Research Topic Hunting for Inflammation Mediators: Identifying Novel Biomarkers for Autoimmune and Autoinflammatory Diseases View all 7 articles

HMGB1: New Biomarker and Therapeutic Target of Autoimmune and Autoinflammatory Skin Diseases

Provisionally accepted
  • 1 College of Life Sciences, Northwest University, Xi'an, Shaanxi, China
  • 2 Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China

The final, formatted version of the article will be published soon.

    High-mobility group box 1 (HMGB1) is expressed in almost all human cells. During cell activation and cell death, the nucleoprotein HMGB1 can translocate to the extracellular space, thus mediating the early inflammatory response as an alarmin or damage-associated molecular pattern (DAMP). Extracellular HMGB1 interacts with immune cells by binding to pattern recognition Toll-like receptors (TLRs), including TLR2 and TLR4, and the receptor for advanced glycation end products (RAGE), thus mediating the immune response to protect the host against pathogens and maintain immune balance. HMGB1 is reportedly upregulated and is a critical biomarker for monitoring disease activity in several chronic inflammatory or autoimmune disorders, including multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, systemic lupus erythematosus and vitiligo. Additionally, the inhibition of HMGB1 expression or its activity has beneficial effects on disease activity in animal models of autoimmune diseases. Thus, HMGB1 is an indispensable biomarker and an important therapeutic target for autoimmune diseases. This review provides a detailed summary of the biological function of HMGB1 and provides a comprehensive outlook in terms of HMGB-focused diagnostic and therapeutic applications in autoimmune skin diseases.

    Keywords: HMGB1, autoimmune skin diseases, Vitiligo, Psoriasis, atopic dermatitis, Alopecia Areata

    Received: 01 Feb 2025; Accepted: 26 Mar 2025.

    Copyright: © 2025 Fan, He, Zhang, Li, Yi and Li. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Xiuli Yi, Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China
    Shuli Li, Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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