Involvement of Regulatory T Cells in the Pathophysiology of Myasthenia Gravis: From a Pediatrician's Perspective

ABSTRACT

Myasthenia gravis (MG) is thought to be primarily caused by autoantibodies targeting proteins at the neuromuscular junction. It has been established that autoantibodies, primarily acetylcholine receptor (AChR) antibodies, act on the neuromuscular junction, impairing neuromuscular transmission or destroying the structure of the neuromuscular junction. However, cellular immunity also plays a significant role, activating various T‐cell subsets and stimulating B cells to produce antibodies, ultimately leading to disease onset. Immune responsiveness changes throughout life. The immune system develops and matures after birth, then declines with age. At each stage, mechanisms protect the body against pathogenic microorganism invasion. It can also lead to conditions where the immune response is insufficient, even against neoplasms formed within the body. This immune response fundamentally operates through the balance between effector T (Teff) cells and regulatory T (Treg) cells. Imbalances in this equilibrium can occur during the course of MG and various other pathologies. Treatment strategies and methods often achieve therapeutic effects by normalizing this balance. In this review, from the perspective of a pediatrician who has long treated patients with not only adult MG but also childhood MG, we would like to discuss the role Treg cells play in regulating this activation of cellular immunity.