| Project/Area Number |
01570206
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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 |
Experimental pathology
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| Research Institution | Tokai University |
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Principal Investigator |
SHIMAMURA Kazuo Tokai University Dept. of Pathology Assistant Professor, 医学部, 講師 (00119679)
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| Co-Investigator(Kenkyū-buntansha) |
HABU Sonoko Tokai University Dept. of Immunology Professor, 医学部, 教授 (30051618)
TAMAOKI Norikazu Tokai University Dept. of Pathology Professor, 医学部, 教授 (50055860)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1990: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | Bone Marrow Transplantation / Hemopoietic Histocompatibility / NK Cell / Bone Marrow Progenitor / Splenic Stromal Cell / Mouse / in vitro / Hybrid resistance / CFUーGM / CFU-M |
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| Research Abstract |
In addition to alloantigens, recipients reject the hemopoietic cells by recognition of surface structures expressed specifically on the hemopoietic cells, when the hemopoietic cells transplanted from a parental donor to F_1 hybrid of other allogeneic recipients. This specific structures called hemopoietic histocompatibility (Hh) are recognized by cells similar to natural killer cells. Molecular structures of Hh antigens, detection of effector cells and the mechanism by which cells bearing these structures are rejected are remained unanswered because most of the experimental system for examining hemopoietic rejection are in vivo assay. The purposes of this project is to make in vitro model of hemopoietic resistance in which donor hemopoietic cells could be eliminated by recognition of their Hh antigens and to clarify the rejection mechanism. We already detected the followings in lastyear : 1) Neither the lineage nor the degree of commitment or differentiation of hemopoietic cells affect
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their expression of Hh antigens. 2) Elimination of grafted progenitors from host spleen commences 3 hours after the transplantation and less than 10 % of progenitors are remained functional by 24 hour. 3) Severity of the rejection is not necessarily due to the difference of allospecificity between hosts and donors. Understanding these evidences, we developed in vitro model of hemopoietic resistance and clarified the followings : 1) Effector cells mediating elimination of hemopoietic progenitors were coenriched with NK activity but not with T cells after passing nylon wool column and applying Percoll density gradient. 2) Suppression of hemopoietic colony growth was abolished by the cytotoxic treatment of effector cells with anti-asial GM1.3) Hemopoietic progenitors in broad range of differentiation and commitment were susceptible in this in vitro assay. And 4) In the presence of host stromal cells, stimulation not but suppression of donor colony growth was observed. From the results, we concluded that suppression of donor hemopoietic colony growth was observed in vitro in the specificity similar to in vivo assay. However, the in vitro elimination of donor hemopoietic progenitors was much weaker than that observed in vivo assay system. Less
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