2016 Fiscal Year Final Research Report
Impaired M2 macrophage function in Behcet's disease as a therapeutic target
Project/Area Number |
26461469
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Collagenous pathology/Allergology
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Research Institution | Nippon Medical School (2015-2016) Yokohama City University (2014) |
Principal Investigator |
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Project Period (FY) |
2014-04-01 – 2017-03-31
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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.
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Free Research Field |
臨床リウマチ学
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