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2016 Fiscal Year Final Research Report

Impaired M2 macrophage function in Behcet's disease as a therapeutic target

Research Project

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Project/Area Number 26461469
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Collagenous pathology/Allergology
Research InstitutionNippon Medical School (2015-2016)
Yokohama City University (2014)

Principal Investigator

Takeno Mitsuhiro  日本医科大学, 医学部, 准教授 (50236494)

Project Period (FY) 2014-04-01 – 2017-03-31
Keywordsベーチェット病 / M1マクロファージ / M2マクロファージ / IL-10 / CCR2
Outline of Final Research Achievements

This study aimed to show a critical role of defective anti-inflammatory M2 macrophage function in Behcet’s disease (BD), because previous studies have shown that defective heme oxygenase-1 (HO-1) expression and IL-10 production are involved in BD. We established in vitro M1 and M2 differentiation systems using GM-CSF and M-CSF, respectively. M2 cells preferentially expressed CCR1, which is also functionally impaired in BD, in addition to HO-1 and IL-10, and migrated more sensitively to MIP-1a than M1 cells. These data suggest that M2 macrophage dysfunction is implicated in development of BD inflammation. Furthermore, in vitro induced M1 cells acquired capacity of IL-10 production in presence of M-CSF, indicating the functional plasicity of macrophages. This findings suggested that phenotypic conversion of macrophages is a promising therapeutic strategy for BD.

Free Research Field

臨床リウマチ学

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Published: 2018-03-22  

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