An imbalance between regulatory T cells and T helper 17 cells in acetylcholine receptor–positive myasthenia gravis patients.

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    • Abstract:
      Abstract: A chronic autoimmune disease, myasthenia gravis (MG) is characterized in 85% of patients by antibodies directed against the acetylcholine receptor (AChR) located at the neuromuscular junction. The functional and effective balance between regulatory T cells (Treg cells) and effector T cells (Teff cells) is lost in the hyperplastic thymus of MG patients with antibodies specific for the AChR (AChR+ MG patients). The objective of this review is to describe how Treg cells and inflammatory T cells participate in this imbalance and contribute to induce a chronic inflammatory state in the MG thymus. We discuss the origins and characteristics of Treg cells and their reported dysfunctions in AChR+ MG patients. We also review the inflammatory condition observed in MG thymus, including overexpression of interleukin (IL)‐1β, IL‐6, and IL‐23, cytokines that promote the differentiation of T helper 17 (TH17) cells and the expression of IL‐17. We summarize the preclinical models used to determine the implication of expression of cytokines, such as IL‐6, IL‐12 (IL‐23 subunit), IL‐17, and interferon γ to the development of experimental autoimmune MG. Finally, we suggest that biological agents, such as humanized monoclonal antibodies that target the IL‐23/TH17 pathway, should be investigated in the context of MG, as they have proven efficiency in other autoimmune diseases. [ABSTRACT FROM AUTHOR]
    • Abstract:
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