1996 Fiscal Year Final Research Report Summary
Mechanism of allograft rejection : moleclar biological analysis of self/nonself recognition
| Project/Area Number |
07670158
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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 |
General medical chemistry
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| Research Institution | Osaka Bioscience Institute |
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Principal Investigator |
YOSHIDA Ryotaro Osaka Bioscience Institute, 4th Dept. , Head, 第4研究部, 部長 (10124760)
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| Co-Investigator(Kenkyū-buntansha) |
VERKHSHA V STA,Tsukita Cell Axis Project, Researcher, 月田細胞軸プロジェクト, 研究員 (80270578)
YAMAMOTO Naoki Gifu University Faculty of Medicine, Assistant Professor, 医学部, 講師 (10260176)
TAKIKAWA Osamu Osaka Bioscience Institute, 4th Dept. , Senior Scientist, 第4研究部, 研究員 (70163342)
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| Project Period (FY) |
1995 – 1996
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| Keywords | self / nonself / cytotoxic T cells / NK cells / macrophages / Histocompatibility antigen / Skin allograft |
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| Research Abstract |
When Meth A fibrosarcoma cells were i. p. injected to C57BL/6 mice, two types of cytotoxic cells [i. e. , CD^<8+> cytotoxic T lymphocytes (CTLs) and macrophages (Mphis) ]infiltrated into the rejection site. The Mphis lysed the allografted tumor cells but were inert toward the donor-type lymphoblasts. By contrast, the CTLs were inactive against transplanted tumor cells, whereas they were cytotoxic against donor-related lymphoblsts. The infiltration of Mphis preceded the infiltration of CTLs by several days during the course of rejection. The tumor cells started to grow within 3 days after transplantation and ceased to grow on day 7 with infiltration of recipient cells including Mphis and CLTs. Rapid elimination of Meth A cells from the peritoneal cavity began around day 9, and by day 12 Meth A cells had been completely rejected from the peritoneal cavity. After the DMDP-liposome treatment, which could effectively and selectively eliminate Mphis from peritoneal exudate cells, there were almost no cytotoxic cells against Meth A cells in the transplantation site and the tumor cells continued to grow there, indicating that a type of Mphi is the effector cell essential for the rejection. Based on these findings, we prepared both effector cells and traget form the graft-graft bed border of skin allograft and detemined the cytotoxic activity of infiltrates (e. g. , Imyphocyte, granulocte and Mphi population) against skin components. The results indicate that the skin damage mediated by allograft-infiltrating cells can be ascribed mainly to Mphis.
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[Publications] W-G.Yu, N.Yamamoto, H.Takenaka, J.Mu, X-G.Tai, J-P.Zou, M.Ogawa, T.Tsutsui, R.Wijesuria, R.Yoshida, S.Herrmann, H.Fujiwara, and T.Hamaoka.: "Molecular Mechanisms Underlying IFN-gamma-mediated Tumor Growth Inhibition Induced during Tumor Immunotherapy with rIL-12." Int. Immunol.8. 855-865 (1996)
Description
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