Immunopathological study on cytokine-producing cells in acute oral mucosal graft-versus-host disease
| Project/Area Number |
11671876
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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 |
病態科学系歯学(含放射線系歯学)
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| Research Institution | Meikai University |
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Principal Investigator |
OHNO Jun Meikai University, School of Dentistry, Research associate, 歯学部, 助手 (10152208)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | ORAL MUCOSAL GVHD / ICAM-1 / CYTOKINES / RT-PCR / IMMUNOHISTOCHEMISTRY / CYTOTOXIC T CELL / INTERFERON-GAMMA / RATS |
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| Research Abstract |
The results obtained were divided into two parts ; 1) roles of cytokines in the induction of acute oral mucosal GVHD, and 2) dynamics of immunocompetent cells, containg cytokine-producing cells. By the RT-PCR methods, both interferon-gamma (IFN) and tumor necrosis factor-alpha (TNF) mRNAs were expressed in the lesional sites at very early stage of oral lesions. The expression of those cytokines was concomitant with immunohistochemical expression of ICAM-1 on the epithelial keratinocytes (KC). These results suggest that local production of IFN and TNF may be responsible for the induction of ICAM-1 expression on KC.Futhermore, the fact that ICAM-1 expression on KC regulates to an infiltration of cytotoxic T cells (CD8-positive cells) into the epithelium, was proved by Stamper-Woodruff binding assay. Of the cytokine-producing cells, we supeculate that NK-like cells and macrophages may be resposible for the production of IFN and TNF, respectively, by in situ hybridization. From these evidences, 'we conclude that NK-like cells and macrophages play important roles in the initiation of acute oral mucosal GVHD.The cytokines produced by those cells may regulate the epitheliotropism of cytotoxic T cell by LFA-1/ICAM-1 binding pathway.
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Report
(3 results)
Research Products
(10 results)
