Lu sur :https://www.ncbi.nlm.nih.gov/pubmed/29405352
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An imbalance between regulatory T cells and T helper 17 cells in acetylcholine receptor-positive myasthenia gravis patients.
Villegas JA1,2,3, Van Wassenhove J1,2,3, Le Panse R1,2,3, Berrih-Aknin S1,2,3, Dragin N1,2,3,4.
Ann N Y Acad Sci. 2018 Feb;1413(1):154-162. doi: 10.1111/nyas.13591. Epub 2018 Jan 24.
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 (TH 17) 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/TH 17 pathway, should be investigated in the context of MG, as they have proven efficiency in other autoimmune diseases.