抗原受体作为b细胞淋巴瘤发展和进化的驱动因素

J. Sepulveda, Noé Seija, P. Oppezzo, Marcelo A. Navarrete
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引用次数: 0

摘要

功能性抗原受体的表达对于正常B淋巴细胞和大多数B细胞肿瘤的细胞存活是必要的。当B细胞受体位点的遗传修饰不能产生功能性抗原受体或导致先前表达的受体发生有害突变时,受影响的B细胞将发生凋亡。产生b细胞受体的三种生理机制,VDJ重组、体细胞超突变和类开关重组,可诱导双链DNA断裂,并可特异性地促进淋巴瘤的发生。另一方面,为正常B细胞提供强大的生存和增殖信号的B细胞受体激活和信号通路可以支持恶性淋巴细胞的生长和进化。因此,从功能的角度来看,一个结构正常的b细胞受体可以表现为一个真正的致癌基因。在本章中,我们深入讨论了最近发现的涉及b细胞受体在淋巴瘤发病机制中的复发机制。讨论围绕两个主要主题:(1)产生功能性抗原受体的遗传机制及其导致致癌事件的错误,以及(2)b细胞受体信号级联的致病性激活。最后,我们将简要评述不同水平靶向b细胞受体的新疗法。
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The Antigen Receptor as a Driver of B-Cell Lymphoma Development and Evolution
The expression of a functional antigen receptor is necessary for cell survival of normal B lymphocytes and most B-cell neoplasms alike. When the genetic modifications of the B-cell receptor locus fail to produce a functional antigen receptor or result in deleterious mutations of a previously expressed receptor, the affected B cell will undergo apoptosis. The three physiological mechanisms that generate the B-cell receptor, VDJ recombination, somatic hypermutation, and class switch recombination, can induce double-strand DNA breaks and can specifically contribute to lymphomagenesis. On the other hand, the B-cell receptor activation and signaling pathways, which provide strong survival and proliferation signals to normal B cells, can support the growth and evolution of malignant lymphocytes. As a result, an otherwise structurally normal B-cell receptor can behave, from the functional perspective, as a true oncogene. In this chapter, we provide an in-depth discussion of the most recently discovered recurrent mechanisms involving the B-cell receptor in lymphoma pathogenesis. The discussion is structured around two major topics: (1) the genetic mecha - nisms that create a functional antigen receptor and their errors leading to oncogenic events, and (2) the pathogenic activation of the B-cell receptor signaling cascade. Finally, we will briefly comment on novel emerging therapies targeting the B-cell receptor at different levels.
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