Immunological mechanisms of liver disturbance in patients with chronic hepatitis C;
| Project/Area Number |
09670527
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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 |
Gastroenterology
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| Research Institution | Fukui Medical University |
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Principal Investigator |
YABU Koji Fukui Medical School, Assistant., 医学部, 助手 (60240793)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 1999: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | Chronic hepatitis C / dendritic cells / recombinant HCV protein / Th2 response / persistent infection |
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| Research Abstract |
We analyzed the antigen-presenting ability of dendritic cells (DCs) originated from peripharal blood leukocytes (PBL) in patients with chronic hepatitis C. One of the possible explanations of HCV persistent infection is insuffisiency of antigen-presenting ability of DCs stimulating HCV specifc T cells. DCs, which were induced co-culturing with high dose of GM-CSF and IL-4, were pulsed with recombinant HCV protein(core or NS3) or peptides and stimulated T cells in vitro. Significantly strong proliferation were observed in HCV-specific T cell responses compared with those of control individuals, but the response in ordinary antigen-specific responses like PPD were weaker than those of the latters. The IL-4 level in culture increase in little proliferating T cell populations, while proliferating T cells stimulated by DCs showed CTL activity against HCV-peptide pulsed target cells. Our results suggested that DCs might induce Th2 type responses as well as Th1 type responses, although these dominancy did not depend upon proper HCV antigens and HLA phenotype. It might be possible that Th2 dominancy against at least some HCV antigen-specific response allowed patients persistent infection.
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Report
(4 results)
Research Products
(3 results)
