Clinical research
FK506 attenuates thymic output in patients with myasthenia gravis
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Submission date: 2010-12-28
Final revision date: 2011-05-05
Acceptance date: 2011-05-11
Online publication date: 2013-12-26
Publication date: 2013-12-31
Arch Med Sci 2013;9(6):1090-1096
Introduction: Myasthenia gravis (MG) is an antibody-mediated, T-cell-de­pendent autoimmune disease. The symptoms are caused by high-affinity IgG against the muscle acetylcholine receptor (AChR) at the neuromuscular junction. The production of these antibodies in B-cells depends on AChR-specific CD4+ T-cells and the thymus gland seems to play a significant role in the pathogenesis of MG. Altered thymic T-cell export seems to be associated with a pathological mechanism in myasthenia gravis. Tacrolimus (FK506) has recently been used to treat MG.
Material and methods: We examined the effects of tacrolimus on thymic T-cell export in patients with MG. Sixteen patients with nonthymomatous and/or thymectomized MG were treated with oral administrations of tacrolimus. To assess the effect of tacrolimus on the thymic output, we assayed the levels of T-cell receptor excision circle (TREC), a molecular marker of thymus emigrants.
Results: T-cell receptor excision circle was not significantly different from those in age-matched controls before tacrolimus therapy, but they were partially decreased 4 months after tacrolimus therapy. T-cell receptor excision circle levels were significantly decreased in the thymomatous group (p < 0.05), but not in the nonthymomatous group. Tacrolimus treatment significantly attenuated TREC levels in cultured CD4-CD8+ cells (p < 0.05), but total cell counts were not significantly changed.
Conclusions: These results indicate that TREC levels may become a marker of the curative effect of tacrolimus therapy for thymomatous MG, and that ta­cro­limus suppresses not only activating T-lymphocytes, but also T-cells.
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