课题基金 / 基金详情

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

Adaptire differentiation of self-Ia-recognition molecules involved in B-B cell interaction
参与 B-B 细胞相互作用的自我 Ia 识别分子的适应性分化
批准号:
61440037
负责人:
HAMAOKA Toshiyuki
金额:
$19.84万
依托单位国家:
日本
项目类别:
Grant-in-Aid for General Scientific Research (A)
财政年份:
1986
资助国家:
日本
项目状态:
已结题
起止时间:
1986 至 1987

项目摘要

项目成果

HAMAOKA Toshiyuki的其他基金

相关文献

中文摘要
翻译
通过本研究,得出以下结论:1.通过识别H-2复合物内的自身I区产物(Ia分子)的B-B细胞相互作用过程参与了由T细胞衍生的B细胞分化因子B151-TRF 2或脂多糖(LPS)诱导的多克隆B细胞分化. B细胞对自身Ia分子的识别是由除表面免疫球蛋白和LFA-1分子以外的尚未确定的分子介导的,所述表面免疫球蛋白和LFA-1分子被报道在免疫系统中起粘附分子的作用。H-2-杂合F1 B细胞显示由至少两个分离的群体组成,其仅识别亲本Ia分子之一。B细胞的Ia识别特异性是“可塑性的”,并由B细胞个体发育过程中存在的辐射敏感骨髓细胞的H-2单倍型决定,而不是由能够决定施加于T细胞上的自身Ia限制特异性的辐射抗性宿主元件决定.发现B细胞表达I-A产物的自我识别受体,但不表达I-E产物.通过利用X-连锁免疫缺陷CBA/N小鼠的B细胞中自身I-A ^k识别分子表达的功能缺陷,通过将P3 U1骨髓瘤细胞与来自缺陷型小鼠的脾细胞融合,建立了能够抑制I-A κ限制性B-B细胞相互作用的单克隆抗体3A 8 -3。用正常(CBA/N x B10.BR)F1雌性脾细胞免疫的(CBA/N x B10.BR)F1(H-2^k)雄性小鼠。
英文摘要
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.
期刊论文(14)
专著(0)
科研奖励(0)
会议论文
Kunio Dobashi: J.Immunol.138. 780-787 (1987)
土桥邦男:J.Immunol.138。
DOI: --
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期刊:
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作者: []
通讯作者:
Shiro Ono: J.Immunol.137. 1149-1156 (1986)
小野四郎:J.Immunol.137。
DOI: --
发表时间:
期刊:
影响因子: --
作者: []
通讯作者:
Shiro Ono: J.Immunol.139. 3213-3223 (1987)
小野四郎:J.Immunol.139。
DOI: --
发表时间:
期刊:
影响因子: --
作者: []
通讯作者:
Shiro Ono: J.Immunol.137. 187-196 (1986)
小野四郎:J.Immunol.137。
DOI: --
发表时间:
期刊:
影响因子: --
作者: []
通讯作者:
共 12 条
    Mechanisms underlying generation and activation of class II MHC-restricted B lymphocytes and their function
    • 批准号:
      02454189
    • 项目类别:
      Grant-in-Aid for General Scientific Research (B)
    • 资助金额:
      $3.97万
    • 财政年份:
      1990
    • 负责人:
      HAMAOKA Toshiyuki
    • 依托单位:
    A site-specific antibody produced with a novel immunization procedure by induction of tolerance to cross-reacting determinants and its utilization in clinical research.
    Analysis of molecular structures of B cell differentiation factors and the corresponding receptors, and their functions.
    • 批准号:
      59440035
    • 项目类别:
      Grant-in-Aid for General Scientific Research (A)
    • 资助金额:
      $12.48万
    • 财政年份:
      1984
    • 负责人:
      HAMAOKA Toshiyuki
    • 依托单位: