ウチダ　ケイコ   UCHIDA Keiko   内田　啓子    所属   医学部 医学科（東京女子医科大学病院）    職種   客員教授
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Vascular-resident CD169-positive monocytes and macrophages control neutrophil accumulation in the kidney with ischemia-reperfusion injury.
掲載誌名	正式名：Journal of the American Society of Nephrology : JASN 略　 称：J Am Soc Nephrol ISSNコード：1533-3450(Electronic)1046-6673(Linking)
巻・号・頁	26(4),pp.896-906
著者・共著者	Karasawa Kazunori†, Asano Kenichi, Moriyama Shigetaka, Ushiki Mikiko, Monya Misa, Iida Mayumi, Kuboki Erika, Yagita Hideo, Uchida Keiko, Nitta Kosaku, Tanaka Masato
発行年月	2015/04
概要	Monocytes and kidney-resident macrophages are considered to be involved in the pathogenesis of renal ischemia-reperfusion injury (IRI). Several subsets of monocytes and macrophages are localized in the injured tissue, but the pathologic roles of these cells are not fully understood. Here, we show that CD169(+) monocytes and macrophages have a critical role in preventing excessive inflammation in IRI by downregulating intercellular adhesion molecule-1 (ICAM-1) expression on vascular endothelial cells. Mice depleted of CD169(+) cells showed enhanced endothelial ICAM-1 expression and developed irreversible renal damage associated with infiltration of a large number of neutrophils. The perivascular localization of CD169(+) monocytes and macrophages indicated direct interaction with blood vessels, and coculture experiments showed that the direct interaction of CD169(+) cell-depleted peripheral blood leukocytes augments the expression levels of ICAM-1 on endothelial cells. Notably, the transfer of Ly6C(lo) monocytes into CD169(+) cell-depleted mice rescued the mice from lethal renal injury and normalized renal ICAM-1 expression levels, indicating that the Ly6C(lo) subset of CD169(+) monocytes has a major role in the regulation of inflammation. Our findings highlight the previously unknown role of CD169(+) monocytes and macrophages in the maintenance of vascular homeostasis and provide new approaches to the treatment of renal IRI.
DOI	10.1681/ASN.2014020195
文献番号	25266072