1987 Fiscal Year Final Research Report Summary
Adaptire differentiation of self-Ia-recognition molecules involved in B-B cell interaction
| Project/Area Number |
61440037
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Immunology
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| Research Institution | Division of Oncogenesis, Depalment of Oncology, Biomedical Research Center, Osaka University Medical School |
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Principal Investigator |
HAMAOKA Toshiyuki Division of Oncogenesis, Biomedical Research Center, Osaka University Medical School Professor, 医学部, 教授 (60028529)
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| Co-Investigator(Kenkyū-buntansha) |
ONO Shiro Division of Oncogenesis, Biomedical Research Center, Osaka University Medical Sc, 医学部, 助手 (80127208)
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| Project Period (FY) |
1986 – 1987
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| Keywords | B-B cell interaction / I-A-region gene products / I-F-region gene products / Self-I-A-recognition specificity / Adaptive differentiation / B cell differentiation factor / Monoclonal antibody / 多クローン性B細胞分化 |
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| Research Abstract |
By this study, the following conclusions were obtained:
1. B-B cell interaction process via recognition of self-I-region products (Ia molecules) within H-2 complex was involved in a polyclonal B cell differentiation induced by a T cell-derived B cell differentiation factor B151-TRF2 or lipopolysaccharide (LPS).
2. The recognition by B cells of self-Ia molecules was mediated by as yet undefined molecules other than the surface immunoglobulin and LFA-1 molecules which are reported to function as adhesion molecules in immune system.
3. H-2-heterozygous Fl B cells were shown to consist of at least two separate populations which recongnize only one of the parental Ia molecules.
4. The Ia-recognition specificity of B cells was "plastic" and determined by the H-2 haplotype of radiation-sensitive bone marrow cells present during B cell ontogeny but not by that of radiation-resistant host elements capable of dictating self-Ia restriction specificity imposed on T cells.
5. B cells were found to express self-recognition receptor for I-A products but not for I-E products.
6. By taking advantage of functional defect(s) in the expression of self-I-A^k recognition molecules in B cells of X-linked immunodeficient CBA/N mice, monoclonal antibody 3A8-3 capable of inhibiting I-A^k-restricted B-B cell interaction was established by fusion of P3U1 myeloma cells with spleen cells from defective (CBA/N x B10.BR)F1(H-2^k) male mice which was immunized with normal (CBA/N x B10.BR)F1 female spleen cells.
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