カトウ ヒデヒト   Kato Hidehito
  加藤 秀人
   所属   医学部 医学科
   職種   助教
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.