INDUCTION OF APOPTOSIS DURING NORMAL AND NEOPLASTIC B-CELL DEVELOPMENT IN THE BURSA OF FABRICIUS
INDUCTION OF APOPTOSIS DURING NORMAL AND NEOPLASTIC B-CELL DEVELOPMENT IN THE BURSA OF FABRICIUS
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DOI：
10.1073/pnas.88.13.5857
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发表时间：
1991-07-01
影响因子：
11.1
通讯作者：
LORING, G
中科院分区：
文献类型：
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作者：
NEIMAN, PE;THOMAS, SJ;LORING, G
胚胎法氏囊滤泡的淋巴细胞参与免疫球蛋白基因的快速生长和免疫前多样化过程。在短期组织培养中，通过机械分散这些细胞破坏滤泡结构，伴随着细胞持续分裂以及大量细胞通过凋亡死亡。在完整滤泡的平行培养中，凋亡受到抑制。γ射线也会在数小时内引发胚胎法氏囊滤泡大量细胞凋亡。由v - myc癌基因诱导的肿瘤前法氏囊干细胞群对滤泡分散和辐射诱导的凋亡高度敏感。相反，在由v - myc和v - rel引发的法氏囊肿瘤中，肿瘤进展伴随着对凋亡诱导的抗性产生。在法氏囊的正常B细胞发育过程中，一个程序性细胞死亡通路可以被激活，并且该通路表达的改变伴随着这个系统中的肿瘤性变化。
The lymphoid cells of embryonic bursal follicles are engaged in rapid growth and preimmune diversification of immunoglobulin genes. Disruption of follicular architecture by mechanical dispersion of these cells in short-term tissue culture was accompanied by continued cell division and extensive cell death by apoptosis. Apoptosis was suppressed in parallel cultures of intact follicles. Gamma-radiation also triggered extensive apoptosis in embryonic bursal follicles within a few hours. Preneoplastic bursal stem cell populations induced by a v-myc oncogene were hypersensitive to induction of apoptosis by follicular dispersion and radiation. In contrast, tumor progression in v-myc- and v-rel-initiated bursal neoplasms was accompanied by development of resistance to induction of apoptosis. A programmed cell death pathway can be activated during normal B-cell development in the bursa, and alterations in the expression of this pathway accompany neoplastic change in this system.