Editors and editing of anti-DNA receptors
Editors and editing of anti-DNA receptors
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DOI：
10.1016/s1074-7613(01)00251-5
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发表时间：
2001-12-01
期刊：
影响因子：
32.4
通讯作者：
Weigert, M
中科院分区：
文献类型：
--
作者：
Li, H;Jiang, YF;Weigert, M
受体编辑是未成熟骨髓B细胞可以自我耐受的一种手段。重（H）和/或轻（L）链基因的重排通过与自身抗原相遇而诱导，以将特异性从自身改变为非自身。我们已经开发了定点转基因小鼠（sd-tg），其转基因编码结合DNA的抗体的H链。表达转基因H链的B细胞主要与小鼠93个功能性VK基因中的4个相关。可能抑制VH结构域与DNA结合的许多天冬氨酸残基区分这些L链VK序列，但接合这些VK编辑器通常需要多次重排。在编辑的B细胞中，有一个亚群是表达多种受体的多特异性细胞。多特异性的一个结果是部分自身反应性;这些多特异性B细胞可能有助于自身免疫。
Receptor editing is a means by which immature bone marrow B cells can become self-tolerant. Rearrangements of heavy (H) and/or light (L) chain genes are induced by encounter with autoantigens to change the specificity from self to nonself. We have developed site-directed transgenic mice (sd-tg) whose transgenes code for the H chain of antibodies that bind DNA. B cells that express the transgenic H chain associate mainly with four of the 93 functional VK genes of the mouse. Numerous aspartate residues that might inhibit DNA binding by the VH domain distinguish these L chain VK sequences, but engaging these VK editors often requires multiple rearrangements. Among the edited B cells is a subset of multispecific cells that express multiple receptors. One consequence of multispecificity is partial autoreactivity; these multispecific B cells may contribute to autoimmunity.