| Project/Area Number |
06454254
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | ASAHIKAWA MEDICAL COLLEGE |
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Principal Investigator |
MAKINO Isao ASAHIKAWA MEDICAL COLLEGE,SECOND DEPARTMENT OF INTERNAL MEDICINE,PROFESSOR OF MEDICINE, 医学部, 教授 (60088854)
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| Co-Investigator(Kenkyū-buntansha) |
HIRANO Fuminori ASSCOCIATE,ASAHIKAWA MEDICAL COLLEGE, 医学部, 助手 (60250552)
TANAKA Hirotoshi ASSISTANT PROFESSOR OF MEDICINE,ASAHIKAWA MEDICAL COLLEGE, 医学部, 講師 (00171794)
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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 |
¥6,800,000 (Direct Cost: ¥6,800,000)
Fiscal Year 1995: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥4,700,000 (Direct Cost: ¥4,700,000)
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| Keywords | bile acids / transcription factors / immunology / molecular biology / gastroenterology / MHC / 免疫応答 / グルココルチコイド / T細胞 / MHC class I / プロテインキナーゼC |
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| Research Abstract |
The immunomodulatory action of bile acids was studied with special reference to
1) regulation of MHC class I & II gene expression,
2) interplay between the glucocorticoid receptor and bile acids,
3) effects of bile acids on T cell signaling.
1) Bile acids were shown to upregulate gene expression of MHC class I,the mechanism for which is suggested to be activation of protein kinase C.Currently, isoform analysis of bile acidrelated protein kinase C is ongoing. Concerning MHC class II gene expression, bile acid ursodeoxycholic acid represses upregulatory effect of IFN-gamma, and this repression is shown to be mediated ligand-independent activation of the glucocorticoid receptor by ursodeoxycholic acid.
2) bile acid ursodeoxycholic acid is shown to activated cytosolic latent glucocorticoid receptor into functional species in the absence of ligands. The molecular mechanism is unknown.
3) Already we have obtained preliminary data suggesting influence of bile acids on the intracellular signaling events in antigen-activated T cells.
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