加藤　秀人    Department   Center for Medical and Nursing Education, Center for Medical and Nursing Education    Position
Article types	Original article
Language	English
Peer review	Peer reviewed
Title	Possible role of LECT2 as an intrinsic regulatory factor in SEA-induced toxicity in d-galactosamine-sensitized mice.
Journal	Formal name：Clinical immunology (Orlando, Fla.) Abbreviation：Clin Immunol ISSN code：15216616
Domestic / Foregin	Foregin
Volume, Issue, Page	137(3),pp.311-321
Author and coauthor	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*
Authorship	Lead author
Publication date	2010/12
Summary	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.