Pelanda Roberta, Torres Raul M
Integrated Department of Immunology, National Jewish Medical and Research Center and University of Colorado Health Sciences Center, 1400 Jackson Street, Denver, CO 80206, USA.
Curr Opin Immunol. 2006 Apr;18(2):184-90. doi: 10.1016/j.coi.2006.01.005. Epub 2006 Feb 3.
Receptor editing has emerged from its original identification as a minor secondary mechanism of B cell tolerance to be considered as a dominant mechanism by which autoreactive immature B cells are rendered tolerant. Clonal deletion, previously regarded as the major mechanism of central B cell tolerance, has been shown by recent studies to operate secondarily and only when receptor editing is unable to provide a non-autoreactive specificity. Receptor editing has also been shown to operate during the development of wild-type B lymphocytes, and ongoing investigations demonstrate the influence of particular signaling molecules in the induction and/or inhibition of receptor editing. Together, these studies begin to map the signaling pathways that regulate receptor editing in autoreactive and non-autoreactive immature B cells.
受体编辑最初被认为是B细胞耐受的一种次要辅助机制，如今已成为使自身反应性未成熟B细胞产生耐受的主要机制。克隆清除曾被视为中枢B细胞耐受的主要机制，但最近的研究表明，它仅在受体编辑无法产生非自身反应性特异性时才作为次要机制发挥作用。研究还表明，受体编辑在野生型B淋巴细胞发育过程中也会发生，并且正在进行的研究揭示了特定信号分子在诱导和/或抑制受体编辑中的作用。这些研究共同勾勒出了调节自身反应性和非自身反应性未成熟B细胞中受体编辑的信号通路。
