Myasthenia gravis (MG) and the experimental autoimmune MG (EAMG) animal model are characterized by T-cell-induced and B-cell-dominated autoimmune diseases that affect the neuromuscular junction. Several subtypes of CD4⁺ T cells, including T helper (Th) 17 cells, follicular Th cells, and regulatory T cells (Tregs), contribute to the pathogenesis of MG. However, increasing evidence suggests that CD8⁺ T cells also play a critical role in the pathogenesis and treatment of MG.

Herein, we review the literature on CD8⁺ T cells in MG, focusing on their potential effector and regulatory roles, as well as on relevant evidence (peripheral, in situ, cerebrospinal fluid, and under different treatments), T-cell receptor usage, cytokine and chemokine expression, cell marker expression, and Treg, Tc17, CD3⁺CD8⁺CD20⁺ T, and CXCR5⁺ CD8⁺ T cells.

Further studies on CD8⁺ T cells in MG are necessary to determine, among others, the real pattern of the Vβ gene usage of autoantigen-specific CD8⁺ cells in patients with MG, real images of the physiology and function of autoantigen-specific CD8⁺ cells from MG/EAMG, and the subset of autoantigen-specific CD8⁺ cells (Tc1, Tc17, and IL-17⁺IFN-γ⁺CD8⁺ T cells). There are many reports of CD20-expressing T (or CD20 + T) and CXCR5⁺ CD8 T cells on autoimmune diseases, especially on multiple sclerosis and rheumatoid arthritis. Unfortunately, up to now, there has been no report on these T cells on MG, which might be a good direction for future studies.