Molecular underpinning of B-cell anergy.
Molecular underpinning of B-cell anergy.
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DOI：
10.1111/j.1600-065x.2010.00936.x
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发表时间：
2010-09
影响因子：
8.7
通讯作者：
Cambier JC
中科院分区：
文献类型：
--
作者：
Yarkoni Y;Getahun A;Cambier JC
多种B细胞特异性库的大量随机产生的副产品是识别自身抗原的细胞的产生。事实上，最近的研究表明，超过一半的主要剧目包括自身反应性B细胞，必须沉默，以防止自身免疫。虽然这种沉默可以通过多种机制发生，但似乎大多数自身反应性B细胞通过无反应性而沉默，其中它们占据外周淋巴器官并继续表达未被占据的抗原受体，但对抗原刺激无反应。在这里，我们审查的分子机制，似乎在维持无反应性B细胞的抗原无反应性。此外，我们提出了新的数据表明，无能的B细胞动员钙在抗原刺激的失败是不介导的失活的基质相互作用分子1，一个关键的中介细胞内存储耗尽诱导的钙离子内流。
A byproduct of the largely stochastic generation of a diverse B-cell specificity repertoire is production of cells that recognize autoantigens. Indeed, recent studies indicate that more than half of the primary repertoire consists of autoreactive B cells that must be silenced to prevent autoimmunity. While this silencing can occur by multiple mechanisms, it appears that most autoreactive B cells are silenced by anergy, wherein they populate peripheral lymphoid organs and continue to express unoccupied antigen receptors yet are unresponsive to antigen stimulation. Here we review molecular mechanisms that appear operative in maintaining the antigen unresponsiveness of anergic B cells. In addition, we present new data indicating that the failure of anergic B cells to mobilize calcium in response to antigen stimulation is not mediated by inactivation of stromal interacting molecule 1, a critical intermediary in intracellular store depletion-induced calcium influx.