Adaptire differentiation of self-Ia-recognition molecules involved in B-B cell interaction

点击翻译按钮获取中文摘要

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.