Receptor editing in self-reactive bone marrow B cells.
Receptor editing in self-reactive bone marrow B cells.
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DOI：
10.1084/jem.177.4.1009
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发表时间：
1993-04-01
期刊：
影响因子：
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通讯作者：
Nemazee D
中科院分区：
文献类型：
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作者：
Tiegs SL;Russell DM;Nemazee D
免疫学的一个中心范式是克隆选择：产生显示克隆分布的抗原受体的淋巴细胞，然后由抗原选择生长或消除。在这里，我们表明，在转基因抗H-2Kk，b抗体基因的小鼠中，发育中的B细胞的同源克隆可以分析自身抗原相遇的结果，诱导骨髓中与自身抗原结合的表面免疫球蛋白M+/独特型+未成熟B细胞改变其抗原受体的特异性。遇到膜结合的KB或KK蛋白的转基因骨髓B细胞通过表达V(D)J重组酶激活基因和组装内源性编码的免疫球蛋白轻链可变基因来修饰其受体。这种(自身)抗原引导的新生成淋巴细胞的特异性改变称为受体编辑。
A central paradigm of immunology is clonal selection: lymphocytes displaying clonally distributed antigen receptors are generated and subsequently selected by antigen for growth or elimination. Here we show that in mice transgenic for anti-H-2Kk,b antibody genes, in which a homogeneous clone of developing B cells can be analyzed for the outcome of autoantigen encounter, surface immunoglobulin M+/idiotype+ immature B cells binding to self-antigens in the bone marrow are induced to alter the specificity of their antigen receptors. Transgenic bone marrow B cells encountering membrane-bound Kb or Kk proteins modify their receptors by expressing the V(D)J recombinase activator genes and assembling endogenously encoded immunoglobulin light chain variable genes. This (auto)antigen-directed change in the specificity of newly generated lymphocytes is termed receptor editing.