| Project/Area Number |
13670581
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | National Institute of Infectious Diseases |
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Principal Investigator |
YAMAGOE Satoshi National Institute of Infectious Diseases, Bioactive Molecules, Senior Researcher, 生物活性物質部, 主任研究官 (00212283)
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| Project Period (FY) |
2001 – 2003
|
| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2003: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | LECT2 / Cytokine / Hepatitis / Concanavalin A / concanavalin A / NKT細胞 |
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| Research Abstract |
LECT2 (leukocyte cell-derived chemotaxin 2) was originally identified for its possible chemotactic activity against human neutrophils in vitro. It is a 16-kDa protein that is preferentially expressed in the liver. Its homologues have been widely identified in many vertebrates. Current evidence suggests that LECT2 may be a multifunctional protein like cytokines. However, the function of LECT2 in vivo remains unclear. To elucidate the role of this protein in vivo, we have generated LECT2-deficient (LECT2^<-/->) mice. We found that the proportion of natural killer T (NKT) cells in the liver increased significantly in LECT2^<-/-> mice, although those of conventional T cells, NK cells, and other cell types were comparable with those in wild-type mice. Consistent with increased hepatic NKT cell number, production of IL-4 and IFN-_Y was augmented in LECT2^<-/-> mice upon stimulation with α-galactosylceramide (α-GalCer), which specifically activates Vα14^+ NKT cells. In addition, NKT cell-mediated cytotoxic activity against syngeneic thymocytes also increased in hepatic mononuclear cells obtained from LECT2^<-/-> mice in vitro. Interestingly, the hepatic injury was exacerbated in LECT2^<-/-> mice upon treatment with Con A, possibly because of the significantly higher expression of IL-4 and Fas ligand. These results suggest that LECT2 might regulate the homeostasis of NKT cells in the liver, and might be involved in the pathogenesis of hepatitis.
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