1993 Fiscal Year Final Research Report Summary
Prevention of pulmonary allograft rejection by treatment with antibodies to LFA-1 and ICAM-1.
| Project/Area Number |
04670821
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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 |
Thoracic surgery
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| Research Institution | Niigata University |
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Principal Investigator |
HIRONO Tatshuhiko Niigata University School of Medisin 2nd Department of Surgery Assistant Professor, 医学部, 助教授 (60092722)
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| Co-Investigator(Kenkyū-buntansha) |
YAMATO Yasusi Niigata University School of Medicin 2nd Department of Surgery Assistant, 医学部・附属病院, 助手 (40240048)
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| Project Period (FY) |
1992 – 1993
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| Keywords | Pulmonary transplantation / LFA-1 / ICAM-1 / Monoclonal antibody / Rat / 拒絶反応 / ラット |
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| Research Abstract |
The key problem encountered following organ transplantation is the allogeneic immune response, which ultimately leads to graft rejection. T cells are thought to be the main effector cells which mediate graft rejection. The activation of T cells is thought to require at least two distinct signals, antigen specific signal delivered via the TCR, as well as a co-stimulatory signal which enables the cell to proceed to IL-2 producion and proliferation. In the absence of the co-stimulatory signal, the T cell makes only a partial response and enters unresponsive state. In the present study, we investigated whether the treatment with antibodies to LFA-1 and ICAM-1 could prevent pulmonary allograft rejection in rats. In BN to LEW combination, pulmonary allograft was rejected within 7 days. In the immunohistochemical study, LFA-1-positive lymphocytes increased in the course of rejection. Two color flow cytometry analysis revealed that the intensity of LFA-1 and ICAM-1 molecules on the infiltrating T cells in the allograft increased. In the cardiac allograft, treatment with antibodies to LFA-1 and ICAM-1 could not prevent graft rejection completely. However graft survival of rats with mAbs was longer than that of rats without treatment. We are now investigating the ettects of mAbs in pulmonary transplantation.
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