| Project/Area Number |
09670481
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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 |
内科学一般
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| Research Institution | Saga Medical School |
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Principal Investigator |
NAGASAWA Kohei Saga Medical School, Internal Medicine, Professor, 医学部, 教授 (00108721)
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| Co-Investigator(Kenkyū-buntansha) |
KOARADA Shuichi Saga Medical School, Internal Medicine, Instructor, 医学部, 助手 (50304887)
USHIYAMA Osamu Saga Medical School, Internal Medicine, Instructor, 医学部, 助手 (40253596)
TADA Yoshifumi Saga Medical School, Internal Medicine, Instructor, 医学部, 助手 (70284627)
SUZUKI Noriaki Saga Medical School, Internal Medicine, Assistant Professor, 医学部, 講師 (40244024)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1998: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1997: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | SjS / HTLV-1 / membrane TNF-alpha / Ig production / T cells / B sells / RP105 / apoptosis / SjS / Ig産生 / シェ-グレン症候群 |
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| Research Abstract |
Sjogren's syndrome(SjS) is characterized by increased production of polyclonal immunoglobulins(Ig) including autoantibodies, in which both T and B cells are highly activated. We demonstrated that human T cells, when infected with HTLV-1 in vitro, were induced to express the 26kDa membrane TNF-alpha. The infected T cells, through this molecule, activated autologous B cells to produce 1gM, which was inhibited by anti-TNF-alpha antibody. It was also found that anti-TNF-alpha antibody induced [Ca^2^+] mobilization in the infected T cells leading to IL-2 and IFN-gamma secretion. Histopathological examinations revealed that T cells having the membrane TNF-alpha were increased in the salivary gland of the patients with SjS.These results indicate that HTLV-1 infection in T cells may stimulate T cells as well as 13 cells through membrane TNF-alpha and that the possibility of the association of HTLV-1 infection with SjS has been raised.
RP105, a novel molecule which has recently been identified on virtually all mature B cells, is known to be related to the B cell proliferation or apoptosis. We found that RPIO5-negative B cells which were hardly found in normal subjects were increased to significant levels. Interestingly, the percentage of RP1O5-negative B cells was elevated in parallel with the increase of the disease activity. In addition, the analysis of other surface markers revealed that the RP1O5-negative B cells might correspond to the highly activated B cells which were involved in the production of 1g. Moreover, the RP1O5-negative B cells tended to be induced to apoptosis by corticosteroids.
These results of the investigation on T and B cells may lead to the clue of the pathogenesis of SjS.
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