2002 Fiscal Year Final Research Report Summary
Elucidation of new adhesion mechanism between neutrophils and gingival epithelial cells via thrombomodulin
| Project/Area Number |
13672193
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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 |
Periodontal dentistry
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| Research Institution | Kagoshima University |
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Principal Investigator |
MATSUYAMA Takashi Kagoshima University, Dental School, Research Associate, 歯学部, 助手 (40253900)
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| Co-Investigator(Kenkyū-buntansha) |
YOTSUMOTO Yukiharu Kagoshima University, Dental School, Research Associate, 歯学部, 助手 (20295265)
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| Project Period (FY) |
2001 – 2002
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| Keywords | Oral epithelial cells / Thrombomodulin / Lymphocytes / Neutrophils / Enzymes |
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| Research Abstract |
Released thrombomodulin has been detected in gingival crevicular fluid with periodontitis from periodontal patients. Gingival epithelial cells express thrombomodulin on their cell surface. In the present study, we investigated the influence of epithelial thrombomodulin by neutrophil protease and the immunoresponse of T lymphocytes in peripheral tissue by the difference of cell density. Neutrophil protease, Elastase but not cathepsin G, released thrombomodulin on oral epithelial cells. The effects occurred in the early phase. On the other hand, released thrombomodulin in the early phase was not related with cytotoxicity by elastase.
T cell contact density in peripheral tissues is less than that in lymphoid organs or in the blood stream. The lower density of T cells in peripheral tissues raises a question as to whether the responses of solitary T cells in peripheral tissue are maintained in the same manner as T cells which are more consistently in contact with one another. We investigated the significance of cell-cell contact in the maintenance of T cell response related to TCR/CD28 signaling. The loss of the cell-cell contact results in the induction of a state of unresponsiveness of T cells and the tyrosine phosphorylation through ICAM-1 by cell-cell contact CD54 in advance seemed to be necessary to maintain T cell response to CD3/CD28 signaling
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