首页> 外文期刊>The journal of immunology >Enforced bcl-xL Gene Expression Restored Splenic B Lymphocyte Development in BAFF-R Mutant Mice
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Enforced bcl-xL Gene Expression Restored Splenic B Lymphocyte Development in BAFF-R Mutant Mice

机译:强制的bcl-xL基因表达恢复BAFF-R突变小鼠的脾脏B淋巴细胞发育。

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The TNFR family member BAFF-R facilitates peripheral B cell development, although it is unclear whether it promotes survival of B cells, or also initiates a differentiation program. We show that disruption of the BAFF-R encoding gene Tnfrsf13c in strain A/WySnJ mice causes a progressive decline in peripheral B cell numbers, beginning at the transitional 1 developmental stage and continuing through the mature peripheral B cell stage. Bcl-xL overexpression in A/WySnJ B cells decreased the turnover of transitional B cells, as determined by 5-bromo-2′-deoxyuridine labeling, and restored follicular B cell development. We conclude that the mutant A/WySnJ allele of Tnfrsf13c can be complemented through the survival signal provided by Bcl-xL.
机译:TNFR家族成员BAFF-R促进外周B细胞发育,尽管尚不清楚其是否促进B细胞存活或是否还启动分化程序。我们显示破坏菌株A / WySnJ小鼠中的BAFF-R编码基因Tnfrsf13c的破坏会导致外周B细胞数量的逐渐减少,从过渡1发育阶段开始,一直持续到成熟的外周B细胞阶段。 Bcl-xL在A / WySnJ B细胞中的过表达降低了过渡B细胞的更新,这是通过5-bromo-2'-deoxyuridine标记确定的,并恢复了滤泡B细胞的发育。我们得出的结论是,Tnfrsf13c的突变A / WySnJ等位基因可以通过Bcl-xL提供的生存信号进行补充。

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