| Project/Area Number |
01570418
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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 | Hokkaido University |
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Principal Investigator |
ABE Shosaku Hokkaido University School of Medicine Associate Professor, 医学部, 助教授 (60113510)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAGUCHI Etsuro Hokkaido University Medical Hospital Instructor, 医学部附属病院, 助手 (10201831)
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| Project Period (FY) |
1989 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1991: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1990: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1989: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | Sarcoidosis / HLA / T cell receptor / RFLP / Disease susceptibility / Tcell receptor / サザンブロックティング / サザンブロッティング / サイルコイド-シス |
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| Research Abstract |
Sarcoidosis is a systemic granulomatous disease with unknown etiology. The pathogenesis of sarcoidosis still remains unclear, but some examinations indicate an immunologic disorder of the patients or the existence of genetic mechanisms. We previously reported a significant association with HLA-DRw52 atitigeri in sarcoidosis. In this study, we performed RFLP analysis of HLA genes arid T cell receptor genes in patients with sarcoidosis. DNA was extracted from peripheral blood lymphocytes of the patients and healthy control subjects. The probes used were cDNA of HL-DRbeta, DQalpha(and DQbeta and T cell receptor alpha and beda chain.
The RFLP analysis could detect polymorphism of the HLA-DRbeda gene that was not distinguishable by conventional serological typing. Five restriction fragments of DRbeda gene were only seen in DRw52-positive individuals, and snowed greater frequencies in the patients than in control subjects, although no restriction fragments were specific for sarcoidosis. The patterns of the fragments in exact individual resembled one another, and patients could be divided into two groups according to the presence of the fragments. The RFLP analysis of DQalpha and DQbeta genes also could more minute polymorphism than serological metliods, but a distinct association of DQ genes was not observed. These results indicate that DR antigens play a major role in the pathogenesis of sarcoidosis.
As for T cell receptor genes, no specific rearrangement of V region were observed in sarcoidosis patients. Restriction fragments of T cell receptor genes snowed no significant difference in the frequencies between the patients and control subjects. These results suggest that there may be heterogenous antigens that cause sarcoidosis.
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