| Project/Area Number |
59480339
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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 |
Otorhinolaryngology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
SAITO Yozo Tokyo Medical and Dental University ・Assistant Professor, 医学部, 助教授 (30014070)
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| Co-Investigator(Kenkyū-buntansha) |
SASAZUKI Takehiko Kyushu University・ Professor, 生体防御医学研究所, 教授 (50014121)
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| Project Period (FY) |
1984 – 1986
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| Project Status |
Completed (Fiscal Year 1986)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 1986: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1985: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1984: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Immune suppression gene / Immune response gene / HLA / IgE / Suppressor T cells / Cryptomeria pollinosis / Allergy |
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| Research Abstract |
The objective of this study was to analyze the immune suppression gene for Cryptomeria janonica pollen antigen (Is-CPAg), which was shown in our previous study to be HLA-linked. We first established an assay system for the measurement of small amounts of anti-CPAg IgE antibody, both in an antigen-specific and isotype-specific manner, and a culture system to induce antigen-driven IgE antibody synthesis in vitro. By using these methods, we clarified that the function of the HLA-DR molecule in the CPAg-driven IgE response is the product of immune response gene, because anti-HLA-DR monoclonal antibody blocked the response, and the interaction between monocyte and monocyte-depleted PBL was restricted by HLA-DR. Furthermore, specific immune response was restored by anti-HLA-DQ monoclonal antibody, suggesting that the HLA-DQ molecule is the product of Is-CPAg. Moreover, 4B4 moleculeson activated <CD4^+> T cells were involved in immune suppression as a target molecule for suppressor T cells or suppressor factors. These observations elucidated the molecules that work not only as a product of Is-CPAg but also as a product for nonspecific interactions in the suppression of IgE response to CPAg.
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