| Project/Area Number |
06670635
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Kurume University |
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Principal Investigator |
OIZUMI Kotaro Kurume Univ.Sch.Med.Professor, 医学部, 教授 (70006097)
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| Co-Investigator(Kenkyū-buntansha) |
HOSHINO Tomoaki Kurume Univ.Sch.Med.Assistant Professor, 医学部, 助手 (00261066)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1994: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | sarcoidosis / CD4^+ T cell / cytokine / CD3 / CD28 / CD80 / CD86 / Second signal / CD4^+ T細胞 / T細胞 / 抗原提示細胞 / BALF / 眼房水 / 抗原刺激 / 結節成形 |
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| Research Abstract |
We investigated surface antigens and spontaneous cytokine production o f T cells from bronchoalveolar lavage fluid (BALF) and aqueous humor (AH) from pulmonary sarcoidosis patients to better understand the role of T cells in granuloma formation. The levels of CD3, CD11b, and CD28 antigen expression on freshly isolated T cells in the BALF of the patients were significantly lower than those in the peripheral blood lymphocytes (PBL) of either sarcoidosis patients or healthy donors (HD). In contrast, the levels of CD80 (B7/B7-1) and CD86 (B70/B7-2) antigen expression were significantly higher on these T cells and alveolar macrophages in the BALF of the patients. Fifty-three T cell clones (TCC) established from the BALF and AH of the three sarcoidosis patients displayd primarily either CD4^+ CD11b^+ CD28^+ or CD4^+ CD11b^- CD28^- phenotypes. A majority (61 to 90%) of these TCC spontancously produced greater amounts of IL-1a, IL-10, TNF,and GM-CSF than did TCC from the PBL from sarcoidosis patients or HD (p<0.05). IFN-g, IL-6, and IL-2, but not IL-4, were also produced by 40 to 48% of these TCC.These results suggest that CD4^+ T cells of the affected organs of sarcoidosis patients are activated and involved in the immunopathogenesis of sarcoidosis through production of various cytokines.
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