Can fingolimod be treatment strategy for myasthenia gravis ?

2014 Fiscal Year Final Research Report

• Project/Area Number: 25870477
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Neurology; Applied pharmacology
• Research Institution: The University of Tokushima
• Principal Investigator: MATSUI Naoko 徳島大学, 大学病院, 診療支援医師 (10547954)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 重症筋無力症 / Finglimod / 胸腺

Outline of Final Research Achievements

We aimed to examine the effect of fingolimod on recent thymic emigrant (RTE). Peripheral blood mononuclear cells were obtained from 4 healthy subjects and 10 patients with multiple sclerosis (MS). Blood sampling for the patients with MS was performed before and after the administration of fingolimod (in 1, 6, and 12 months). CD3+CD4+ T, naive T (CD45RA+, CD45RO-), and memory T cells (CD45RA-, CD45RO+) were identified by FACS. We also analyzed naive T’s expression of CD31, a surrogate marker of RTE. The frequency of memory T cells was relatively increased, but that of RTE was decreased in MS. Effect of fingolimod on RTE continued over one year. Fingolimod act as a potent antagonist at sphingosine 1-phosphate receptor type 1 (S1P1) on lymphocytic emigration from secondary lymphoid organs as well as thymus. In myasthenia gravis (MG), removal of thymus results in RTEs. We speculate that fingolimod have a possibility of the pharmacological effect similar to thymectomy.

Free Research Field

神経免疫