Abstract
Objective: As a classical autoimmune disorder, anti-acetylcholine receptor (AChR) antibody positive myasthenia gravis (MG) has an unconventional pathophysiology that involves thymus, the central organ for immune tolerance induction. Both natural killer (NK) cells and type 17 helper T (Th17) cells possess capacity to influence autoimmune inflammation. This study aims to determine the presence of Th17 and NK cells in the thymus from MG patients. Methods: Thymectomy materials of MG patients and non-MG controls were assessed by CD56, CD16, CD2, CD3, NKG2D, NKp46 and IL-23R flow cytometry and IL-23R, IL-21R, and ROR-γ immunohistochemistry. Results: Even though NK cell infiltration was limited, the majority of these cells displayed activation markers NKG2D and NKp46. Expectedly, the amount of CD2+ lymphocytic cells were higher than CD3+ thymocytes in which a considerable percentage was carrying the receptor for IL-23 (IL-23R). In addition to IL-23R, IL-21R, and ROR-γ were also detected in MG thymus as a marker related to Th17 cells. These Th17-related markers were reduced in thymoma compared to that of detected in thymic hyperplasia or the MG thymus with normal histopathology. Conclusion: Both NK cells and Th17 cells are found in the MG thymus indicating a possible cross-regulation between these cell types that may influence the course of autoimmune reactions.
Highlights
Myasthenia gravis (MG) is a rarely encountered antibody-mediated and CD4+ helper T cell-dependent autoimmune disease of skeletal muscles
Since the interaction between natural killer (NK) cells and Th17 cells has been underlined in autoimmune disorders [16,17], we asked whether these cells are found in the MG thymus
The existence of NK cells and Th17 cells are reported in the thymus of anti-acetylcholine receptors (AChRs) antibody positive MG patients
Summary
Myasthenia gravis (MG) is a rarely encountered antibody-mediated and CD4+ helper T cell-dependent autoimmune disease of skeletal muscles. These antibodies affect neuromuscular junction generally by targeting acetylcholine receptors (AChRs) and lead to muscle weakness [1]. The presence of NK and Th17 in myasthenia gravis thymus secondary lymphoid structures, B lymphocytes, and by NK cells [16,17]; NK cells have been indirectplasma cells in such an organ which is responsible of ly implicated in maintenance of tolerance and sup-. Autore- vious in the disease etiopathology, to date, the presactive antibody production needs to be supported ence of NK and Th17 cells was not reported in the by helper T (Th) cells with certain subtype differen- MG thymus
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