カトウ　ヒデヒト   加藤　秀人    所属   統合教育学修センター 統合教育学修センター    職種   非常勤講師
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Possible role of LECT2 as an intrinsic regulatory factor in SEA-induced toxicity in d-galactosamine-sensitized mice.
掲載誌名	正式名：Clinical immunology (Orlando, Fla.) 略　 称：Clin Immunol ISSNコード：15216616
掲載区分	国外
巻・号・頁	137(3),pp.311-321
著者・共著者	DANG Hang Minh† ,KATO Hidehito† ,UESHIBA Hidehiro† ,OMORI-MIYAKE Miyuki ,YAMAGOE Satoshi ,ANDO Kazuyoshi ,IMANISHI Ken'ichi ,ARIMURA Yutaka ,HARUTA Ikuko ,KOTANI Tohru ,OZAKI Makoto ,SUZUKI Kazuo ,UCHIYAMA Takehiko ,YAGI Junji*
担当区分	筆頭著者
発行年月	2010/12
概要	To elucidate whether leukocyte cell-derived chemotaxin 2 (LECT2) controls the progression of staphylococcal enterotoxin A (SEA)-induced toxicity, we examined the role of LECT2 in a mouse model. Almost all the C57BL/6J (B6) mice survived for 72 h after the injection of 0.1 ug of SEA and 20 mg of d-galactosamine (d-GalN). However, the same treatment protocol in LECT2(-/-) mice produced a high lethality (~90%), severe hepatic apoptosis, and massive hepatic and pulmonary hemorrhage, similar to the situation observed in B6 mice treated with 1.0 ug SEA/d-GalN. The plasma LECT2 levels in B6 mice treated with 1.0 ug SEA/d-GalN were inversely correlated with the plasma cytokine levels and were associated with prognosis. LECT2 administration increased the survival of B6 mice and down-regulated TNF-a and IL-6. These results suggest the involvement of LECT2 in the regulation of fatal SEA-induced toxicity in d-GalN-sensitized mice.