Investigation of biomarkers to select the optimal disease-modifying drugs for each individual patient with multiple sclerosis.

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K21285
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Collagenous pathology/Allergology; Medical pharmacy
• Research Institution: Kyoto Prefectural University of Medicine
• Principal Investigator: Fujii Chihiro 京都府立医科大学, 医学部附属病院, 研究員 (00516065)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: 多発性硬化症 / フィンゴリモド / T細胞 / バイオマーカー

Outline of Final Research Achievements

We found that the frequency of CD56+ T cells in peripheral blood increased in fingolimod-treated patients with multiple sclerosis. These T cells expressed cytotoxic molecules and showed a Th1-like response. In addition, the CD56+ T cells produced IFN-γ in response to myelin basic protein. The elevated frequency of CD56+ T cells in fingolimod-treated patients was further increased at relapse. Relapse-experienced patients retained a higher frequency of CD56+ T cells even during remission compared to patients who did not have any relapse while on fingolimod treatment.
Our results showed that the T cell phenotypes were altered under fingolimod therapy,and raised a possibility that the frequency of CD56+ T cells is a useful biomarker for predicting and detecting relapses, although further confirmation is required.

Free Research Field

神経内科学