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KAKEN_23390217seika.pdf
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Title |
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免疫学的介入による心筋梗塞後リモデリング予防法の開発
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Kana |
メンエキガクテキ カイニュウ ニ ヨル シンキン コウソクゴ リモデリング ヨボウホウ ノ カイハツ
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Menekigakuteki kainyu ni yoru shinkin kosokugo rimoderingu yoboho no kaihatsu
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Developing successful immunomodulatory therapies against ventricular remodeling after myocardial infarction
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佐野, 元昭
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サノ, モトアキ
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Sano, Motoaki
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慶應義塾大学・医学部・准教授
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Research team head
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科研費研究者番号 : 30265798
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Yan, Xiaoxiang
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慶應義塾大学・医学部・大学院
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Research team member
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科研費研究者番号 : 90594979
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安西, 淳
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アンザイ, アツシ
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Romanization |
Anzai, Atsushi
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慶應義塾大学・医学部・助教
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Research team member
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科研費研究者番号 : 50528164
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2014
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科学研究費補助金研究成果報告書
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2013
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Abstract |
樹状細胞、γδT細胞、NK細胞について、心筋梗塞後の炎症、損傷治癒過程における役割について検討した。樹状細胞を除去したマウスでは梗塞後左室リモデリングが増悪し心不全を発症した。γδT細胞はIL-17の分泌を介して好中球の浸潤を遷延化させ、マクロファージを向炎症性>損傷治癒へ傾かせ、線維芽細胞の増殖、collagen産生を促進させ、炎症の慢性化、臓器の破壊を促進させた。心筋梗塞後に肺NK細胞は、IL-10を産生することによって、肺の血管内皮細胞のバリアー機能を維持し、血管内から肺組織への好中球の侵入を抑制していることを明らかにした。
Left ventricular (LV) remodeling leads to chronic heart failure and is a main determinant of morbidity and mortality after myocardial infarction (MI). Mice with DC ablation showed deteriorated LV function and remodeling concomitant with enhanced expression of IL-1beta, IL-18, and TNF-alpha, prolonged extracellular matrix degradation, marked infiltration of proinflammatory monocytes. A deficiency of gamma-delta T cells improved survival, limiting infarct expansion and fibrosis in noninfarcted myocardium and alleviating LV dilatation and systolic dysfunction after MI. IL-17A-producing gamma-delta T cells promotes sustained infiltration of neutrophils and macrophages, , aggravating cardiomyocyte death, and enhancing fibroblast proliferation. Depletion of NK cells from mice exhibited severe respiratory. Adoptive transfer of NK cells from wild-type mice, but not from IL-10 knockout mice, into the NK cell-depleted mice rescued the respiratory phenotype.
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研究種目 : 基盤研究(B)
研究期間 : 2011~2013
課題番号 : 23390217
研究分野 : 医歯薬学
科研費の分科・細目 : 内科系臨床医学・循環器内科
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