1988 Fiscal Year Final Research Report Summary
Analysis of regulatory mechanism for autoantibody production by using human T and B cell clones.
| Project/Area Number |
61480177
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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 |
内科学一般
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| Research Institution | TOHOKU UNIVERSITY |
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Principal Investigator |
SASAKI Takeshi Instructor, Tohoku University School of Medicine, 医学部付属病院, 講師 (50110656)
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| Co-Investigator(Kenkyū-buntansha) |
ENDO Kazuyasu Instructor, Tohoku University School of Medicine, 医学部付属病院, 講師 (60125507)
SUGAMURA Kazuo Professor, Tohoku University School of Medicine, 医学部, 教授 (20117360)
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| Project Period (FY) |
1986 – 1988
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| Keywords | anti-DNA antibody / B cell clone / T cell clone / autoantibody / 全身性エリテユトーデス |
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| Research Abstract |
1. We obtained six human B cell clones producing monoclonal anti-DNA antibodies by clonal transformation methods. anti-DNA idiotypes expressed on these surface of the clones were widely ditributed among human B cell clones. Anti-idiotypic antibody producing clones were also detected in patients with inactive SLE as well as in healthy subjects, indicating the idiotypic regulation of anti-DNA autoantibody production.
2. We established T cell clones expressing anti-DNA idiotypes by using clonaltrasnformation methods, where SLE-drived T cells were cocultured with HTLV-1-infected T cell clones(MT-1 or KAN). The obtained T cell clones, however, failed to have ability to regulate anti-DNA antibody production in vitro. The studies are in progress for obtaining T cell clones responsible for autoantibody production.
3.Anti-idiotypic antibodies to numan anti-DNA antibodies had ability to regulate anti-DNA antibody production in human in vitro. We extended the application of regulatory ability of anti-idiotypic antibody to the therapy of autoimmune diseases in autoimmune mice in vivo. The administration of anti-idiotypic antibodies conjugated with neocarzino-statin brought into the elongation on the survival and the deterioration of development of lupus nephritis in the treated mice.
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