| Project/Area Number |
10470435
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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 Univ. of Dental Hospital., Kyushu University Assoc. Prof., 歯学部・附属病院, 助教授 (20117055)
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| Co-Investigator(Kenkyū-buntansha) |
TERAMOTO Nariyoshi Faculty of Medicine, Kyushu University Res.Assoc., 大学院・医学研究院, 助手 (40294912)
NAKAMURA Seiji Univ. of Dental Hospital., Kyushu University Assist. Prof., 歯学部・附属病院, 講師 (60189040)
吉田 篤哉 九州大学, 歯学部, 講師 (00284521)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥14,500,000 (Direct Cost: ¥14,500,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1998: ¥11,200,000 (Direct Cost: ¥11,200,000)
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| Keywords | HIV / HTLV-I / autoimmune disease / Sjogren's syndrome / Salivary gland / cytokine / T cell / シェーグレン症侯群 / パッチクランプ |
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| Research Abstract |
Measurement of whole salivary flow rate revealed that function of salivary gland is frequently impaired in HIV- or HTLV-I-infected patients. The salivary gland dysfunction observed in these patients was clinically similar to one of autoimmune disease, Sjogren's syndrome. To clarify the etiopathological association of Sjogren's syndrome with HTLV-I, we first of all examined the localization of HTLV-I proviral DNA in the salivary gland of the patients. The results suggested HTLV-I infected T cells accumulate in the salivary glands and are involved in the induction of the salivary gland dysfunction. Cytokines detected in the salivary glands was mainly Th1 cytokines IL-2 and IFNγ produced by CD4-positive T cells. Furthermore, examination of the T cell receptor C gene usage in the salivary glands revealed that T cells expressing unique T cell receptors are accumulated in the salivary glands. These T cells were commonly present in patients with Sjogren's syndrome. These results strongly suggest that a self-reactive T cells could be infected with the virus, activated by the virus, and thereafter induce this type of autoimmune disease. Using a path-clamp method, we found, in rat salivary acinar cells, a K^+ channels which was Ca^<2+>-dependent and voltage-dependent. This report is the first report in the world.
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