2018 Fiscal Year Final Research Report
Identification of kidney disease specific macrophages and its functional analysis and establishment of control method
Project/Area Number |
16K10062
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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 |
Pediatrics
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Research Institution | Fujita Health University |
Principal Investigator |
Ikezumi Yohei 藤田医科大学, 医学部, 准教授 (70361897)
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Co-Investigator(Kenkyū-buntansha) |
矢尾板 永信 新潟大学, 医歯学系, 准教授 (00157950)
山田 剛史 新潟大学, 医歯学総合病院, 助教 (90601922)
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Project Period (FY) |
2016-04-01 – 2019-03-31
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Keywords | 慢性糸球体腎炎 / 慢性腎臓病 / マクロファージ / M2型活性化マクロファージ / 間質線維化 |
Outline of Final Research Achievements |
The progression of chronic lesions such as interstitial fibrosis, as well as macrophage (MQ) accumulation are common futures observed in the course of progressive chronic kidney diseases. This study tried to identify a chronic kidney disease-specific MQ which are associated with chronic lesions irrespective of the nature of the underlying disease. We found that M2-type activated MQs; MQs expressing CD163, CD204, or CD36 as M2-type MQ antigens were involved in the progression of chronic lesions. In particular, CD163+ M2-type MQ as the main MQ population associated with interstitial fibrosis across a range of progressive forms of kidney disease, suggesting a functional role for this MQ subset in renal fibrosis. Since M2-type MQ can be rather activated by glucocorticoid, another immunosuppressive drug such as purine nucleoside antimetabolite might be useful to regulate their activation.
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Free Research Field |
小児腎臓病
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Academic Significance and Societal Importance of the Research Achievements |
本研究により同定された腎慢性病変の進展に関わる腎疾患特異的MQは、全ての慢性腎臓病(CKD)の治療ターゲットであり、その制御法(治療法)の開発は現在まだ進行中の研究課題であるが、現在社会問題となっているCKD患者および透析患者(末期腎不全患者)の増加に歯止めをかけるための活路を見出す課題である
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