Etiological study of oral disease in HIV and HTLV-I positive patients-characteristics of salivary gland cells-

Research Project

Project/Area Number	10470435
Research Category	Grant-in-Aid for Scientific Research (B).
Allocation Type	Single-year Grants
Section	一般
Research Field	Surgical dentistry
Research Institution	Kyushu University
Principal Investigator	ABE Kihachiro Univ. of Dental Hospital., Kyushu University Assoc. Prof., 歯学部・附属病院, 助教授 (20117055)
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)
Project Period (FY)	1998 – 2000
Project Status	Completed (Fiscal Year 2000)
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)
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
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.