REVIEW article
Front. Immunol.
Sec. Inflammation
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1605185
This article is part of the Research TopicPattern Recognition Receptors: Balancing Inflammation and Immune HomeostasisView all 4 articles
TLRs in Asthma: Immune Regulation
Provisionally accepted
- Institute of Immunology and Molecular Medicine, Jining Medical University, Jining, China
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As a chronic inflammatory illness of the respiratory system, asthma occurs due to various factors and is characterized by a T helper 2 (Th2)-skewed immune response, airway hyperresponsiveness, and reversible airflow obstruction. Toll-like receptors (TLRs) perform a "double-edged sword" function in asthma-related immunological dysregulation by recognizing damage-associated molecular patterns and pathogen-associated molecular patterns. In turn, the activation of some TLRs stimulates epithelial cells to release inflammatory cytokines, exacerbating Th2-driven inflammation and contributing to airway remodeling. Certain TLR signals help inhibit allergic responses by inducing type I interferon or regulatory T cells. The TLR family comprises 10 members, each responsible for recognizing the distinct molecular structure of multiple microbial sources. Variations in environmental microbial exposure duration and host genetic background contribute to the complexity of the TLR signaling network during asthma development. In recent years, therapeutic strategies targeting TLRs have shown potential for asthma treatment. However, a comprehensive review of TLRs in asthma is lacking. Therefore, this review sought to examine the functional mechanisms of TLRs and associated signaling cascades in asthma, and explore novel prevention and treatment approaches centered on TLRs modulation.
Keywords: Toll-Like Receptors, Toll-like receptors signaling, Asthma, immune cells, Inflammation, Cytokines, therapeutic strategies
Received: 02 Apr 2025; Accepted: 16 Jun 2025.
Copyright: © 2025 Xu, Yu, Yang, Li, Xiong 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:
Huabao Xiong, Institute of Immunology and Molecular Medicine, Jining Medical University, Jining, China
Chunxia Li, Institute of Immunology and Molecular Medicine, Jining Medical University, Jining, China
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