@techreport{oai:kindai.repo.nii.ac.jp:00014060,
 author = {野﨑,  祐史},
 month = {Jan},
 note = {研究成果の概要（和文):  Tim-1(Kim-1)はCD4+T細胞の免疫応答を調節し, 尿細管障害にて発現する. 今回, 抗Tim-1 抗体(RMT1-10)をループスモデルであるMRL-Faslprマウスに3ヶ月齢から16週間投与した. 結果, 生存率, リンパ節腫脹, 皮疹増悪は改善した. 腎機能, 蛋白尿, 抗DNA抗体産生, リンパ球浸潤程度は改善した. Th1/17免疫応答は低下したが, 制御性Ｂ/Ｔ細胞は増加した. RMT1-10治療群はまた, 糸球体免疫グロブリン・C3沈着, 細胞増殖・アポトーシスも抑制された. 尿中・尿細管Kim-1発現は低下し, 尿細管間質障害は改善した. RMT1-10は治療薬となりうる可能性が考えられた.           研究成果の概要（英文): The T-cell immunoglobulin mucin 1 (Tim-1), (Kim-1), modulates CD4+ T-cell responses and is also expressed by damaged proximal tubules. This study investigated the effects of an inhibitory anti-Tim-1 antibody (RMT1-10) in lupus-prone MRL-Faslpr mice. The mice were treated with RMT1-10 from 3 mo of age for 16 wk. RMT1-10 treatment significantly improved survival, limited the development of lymphadenopathy and skin lesions, preserved renal function and decreased proteinuria, reduced serum anti-DNA antibody levels, and attenuated renal leukocyte accumulation. Th1/Th17 cellular responses were reduced, but regulatory T/B cells were increased. RMT1-10 treatment also reduced glomerular immunoglobulin and C3 deposition and suppressed cellular proliferation and apoptosis. Urinary excretion and renal expression of Kim-1 was reduced, reflecting diminished interstitial injury. As RMT1-10 attenuated manipulating immune system Tim-1 may represent a therapeutic strategy in autoimmune diseases., 研究種目：若手研究(B);  研究期間：2012～2013;   課題番号：24791012;   研究分野：医歯薬学;   科研費の分科・細目：内科系　臨床医学　膠原病・アレルギー内科学, application/pdf},
 title = {ループス腎炎に対する抗Kｉｍ-１抗体の治療効果について},
 year = {2013},
 yomi = {ノザキ, ユウジ}
}