| Project/Area Number |
08671407
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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 |
Digestive surgery
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| Research Institution | Tohoku University |
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Principal Investigator |
SUNAMURA Makoto Tohoku University, hospital Reserch Associate, 医学部・附属病院, 助手 (10201584)
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| Co-Investigator(Kenkyū-buntansha) |
KOBARI Masao Tohoku University, School of med.Lecturer, 医学部, 講師 (30170369)
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| Project Period (FY) |
1996 – 1997
|
| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1997: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1996: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Islet transplantation / IL-12 / anti IL-12 antibody / Th1 / Th2 / ICAM-1 / LFA-1 / IL-12,p40遺伝子 / Th2バランス / 血管新生 |
|---|
| Research Abstract |
The classification of T helper cell subsets into Th1 and Th2 populations based on the production of specific cytokines has been useful to understand various immune reactions. IL-12 drives the development of Th1 cells and inhibits the generation of Th2 cells. The role of LL-12 in the acute allograft rejection is still unclear. In this study, we examined the influence of rat anti-mouse-IL-12 mAb (C 17.8) on mouse islet allograft (ICR*C57BL/6) survival. Postoperative intraperitoneal administration of C 17.8 mAb significantly prolonged islet allograft survival as compared with graft survival in untreated mice. The rejection in untreated recipients was characterized by intragraft IFN-gamma and IL-2 gene expressions, not IL-4 or IL-10, indicating Th1 response. C 17.8 mAb therapy impaired intragraft Th1 cytokine (IFN-gamma and IL-2) gene expression on day 4, 8 post-transplant and enhanced IL-10 expression on day 4. Further, it decreased IFN-gamma production from splenocytes in vivo sensitized after transplantation. These findings indicate that post-transplant systemic administration of C 17.8 mAb can prevent islet allograft rejection, which results from the blockade of Th1-mediated response.
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