1994 Fiscal Year Final Research Report Summary
Mechanism of allograft rejection : molecular biological analysis of self/nonself recognition
| Project/Area Number |
05680538
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Structural biochemistry
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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) |
USHIO Yumiko Osaka Bioscience Institute, 4th Dept., Research Associate, 第4研究部, 研究員 (90193862)
YAMAMOTO Naoki Osaka Bioscience Institute, 4th Dept., Research Associate, 第4研究部, 研究員 (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) |
1993 – 1994
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| Keywords | self / nonself / transplantation / recognition / major histocompatibility complex / macrophage / monoclonal antibody / congenic mice / rejection |
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| Research Abstract |
The great survival value of acquired immunity is self-evident. Central to aquired immunity is the recognition of the distinction between "self" and "nonself." Acquired immunity is invoked against a foreign invader, with the ultimate goal of eliminating the foreign material.
In this project, we tried (1) to establish the method to recover almost all the cells infiltrating into the transplantation site, (2) to identify the type of cells cytotoxic against the transplants, (3) to determine the recognized molecule (s) on the transplants, and (4) to elucidate the recognition molecule (s) on the effector cells.
The results which we have obtained during recent 2 years are as follows. (1) We transplanted Meth A tumor cells into the peritoneal cavity of C57BL/6 mouse. The tumor cells are ascites type, and therefore, by lavage of the mouse peritoneal cavity, we could obtain almost all the leukocytes infiltrating into the rejection site. The major population of cytotoxic cells against allografted Meth A cells was found to be a type of macrophages. (2) We demonstrated that the allograft-induced macrophages (AIM) are able to recognize MHC class I molecules on allogeneic cells as nonself. (3) We have isolated a monoclonal antibody (K16.5) specific for AIM and cDNAs encoding the K16.5 antigen. (4) Surprizingly, AIM were highly cytotoxic not only against allografted tumor cells but also against nonself lymphoblasts. AIM were also cytotoxic against non-MHC-disparate nonself lymphoblasts. These results coincide well with the clinical findings in transplantation immunity.
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