| Project/Area Number |
07457492
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | Kyushu University |
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Principal Investigator |
ABE Kihachiro Kyushu University, Dentistry, Assoc.Professor, 歯学部, 助教授 (20117055)
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| Co-Investigator(Kenkyū-buntansha) |
KUBOTA Yasutaka Kyushu University, Dentistry, Assistant, 歯学部, 助手 (60205151)
NAKAMURA Seiji Kyushu University, Dentistry, Assist.Professor, 歯学部, 講師 (60189040)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥7,800,000 (Direct Cost: ¥7,800,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1995: ¥6,900,000 (Direct Cost: ¥6,900,000)
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| Keywords | HIV / HTLV-I / salivary gland / cytokine / T cell / Sjogren's syndrome / autoimmune disease / HTLV-1 |
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| Research Abstract |
The involvement of Human T lymphotrophic virus type I (HTLV-I) in the pathogenesis of Sjogren' syndrome (SS), which is also seen in HIV-infected patients, was clarified in this study.
Eleven of one hundred and three SS patients, who were serologically HTLV-I positive, referred to the Second Department of Oral and Maxillofacial Surgery, Kyushu University Dental Hospital between 1992 and 1996, were studied. A polymerase chain reaction (PCR) amplification of cellular DNA revealed that the cellular DNA extracted from the labial salivary glands (SG) contained full HTLV-I proviral DNA in the SG.In situ PCR hybridization which detect HTLV-I proviral DNA in the section of the SG demonstrated HTLV-I proviral DNA in the nucleus of the infiltrating T cells, but not in either salivary gland epithelial or acinar cells. Quantification of HTLV-I proviral DNA was performed using MT2 cells, a human HTLV-I -infected T cell line and salivary gland epithelial cell lines, and revealed that the viral loads in the SG were approximately 8 times to 9 * 10^4 times higher than those in the peripheral blood mononuclear cells.
An accumulation of HTLV-I-infected T cells in the SG is thus suggested. HTLV-I likely cause the self-reactive T cells proliferate and, as a result, thereafter induced SS.
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