谷氨酰胺如何保护眼肌型重症肌无力？2024最新T细胞免疫机制解析

As previously mentioned, unlike conventional myasthenia gravis (MG), patients with localized ocular myasthenia gravis (LOMG) exhibit a significant reduction in the proportion of mucosa-associated invariant T cells and naive CD8⁺ T cells. This characteristic may provide a mechanistic explanation for the protective effect of glutamine on LOMG. Glutamine is a critical nutrient highly dependent by immune cells, particularly crucial for the regulation of T cell subsets. Effector T cells are highly dependent on glutamine to meet the demands of rapid proliferation, while the differentiation and functional maintenance of regulatory T cells are also influenced by it (DOI: 10.1016/j.smim.2016.09.003). Additionally, glutamine metabolism is involved in regulating the balance between Th17 and Treg cells, and the imbalance of Th17/Treg is a core immunopathological feature of various autoimmune diseases (DOI: 10.1038/s41423-023-01036-7; DOI: 10.1007/s11427-020-1703-2). Therefore, the protective effect of glutamine on LOMG may be achieved through the regulation of T cell subset homeostasis and inhibition of autoimmune reactions, directly combating peripheral immune dysregulation in LOMG. Research on the tumor microenvironment also provides supporting evidence, as the availability of glutamine directly impacts the function of CD8⁺ T cells (DOI: 10.1096/fj.202403019R), which resonates with the characteristic reduction in naive CD8⁺ T cells in LOMG patients, suggesting that glutamine may exert its protective effect by maintaining CD8⁺ T cell homeostasis. Furthermore, glutamine, as a common fitness supplement, promotes muscle protein synthesis and accelerates post-exercise recovery (DOI: 10.1186/s12986-024-00820-0), indicating that it may also protect LOMG through multiple pathways, such as enhancing skeletal muscle function and improving neuromuscular junction metabolism support.