REVIEW article
Front. Immunol.
Sec. Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders
Toll-Like Receptors and Their Role in the Pathogenesis of Myasthenia Gravis: A Comprehensive Review
Provisionally accepted- Department of Neurology, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua Medicine, Tsinghua University, Beijing, China
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Myasthenia gravis (MG) is a chronic autoimmune neuromuscular disorder marked by autoantibody-mediated dysfunction at the neuromuscular junction, resulting in fluctuating muscle weakness. The pathogenesis of MG involves a complex interplay between genetic predisposition, environmental factors, and immune system dysregulation. Among these, the innate immune system, particularly Toll-like receptors (TLRs), has emerged as a critical player in disease progression by influencing both innate and adaptive immunity. TLRs are a family of pattern recognition receptors (PRRs) that detect pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), triggering immune responses. Dysregulation of TLRs expression and signaling in MG has been implicated in chronic inflammation, breakdown of immune tolerance, and activation of autoreactive T and B cells. Overexpression of specific TLRs, such as TLR4 and TLR9, has been reported in MG patients, particularly in thymic tissues and peripheral immune cells, correlating with increased pro-inflammatory cytokine production and autoantibody generation. These aberrant responses contribute to the autoimmune cascade that underlies MG. Emerging evidence highlights the therapeutic potential of targeting TLRs pathways in MG. Strategies include using TLRs antagonists, modulating downstream signaling pathways, and leveraging epigenetic regulators to normalize TLRs activity. This review examines the role of TLRs in MG by exploring their expression profiles, their involvement in inflammatory signaling pathways, their impact on the adaptive immune system, and their potential as therapeutic targets. A better understanding of the role of TLRs in MG pathogenesis could open new avenues for modulating immune responses and precision therapies targeting the innate immune system.
Keywords: Myasthenia Gravis, Toll-Like Receptors, Cytokine release, therapeutic targets 1, Autoimmune neuromuscular disorders
Received: 08 May 2025; Accepted: 02 Dec 2025.
Copyright: © 2025 Zheng, Li, Ma, Zhu, Li and Feng. 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: Xinhong Feng
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.
