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首页> 外文期刊>Cellular immunology >Type I interferon (IFN-alpha/beta) rescues B-lymphocytes from apoptosis via PI3Kdelta/Akt, Rho-A, NFkappaB and Bcl-2/Bcl(XL).
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Type I interferon (IFN-alpha/beta) rescues B-lymphocytes from apoptosis via PI3Kdelta/Akt, Rho-A, NFkappaB and Bcl-2/Bcl(XL).

机译：I型干扰素（IFN-α/β）通过PI3Kdelta / Akt，Rho-A，NFkappaB和Bcl-2 / Bcl（XL）使B淋巴细胞免于凋亡。

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摘要

Although IFN-alpha was reported to promote the survival of peripheral B-lymphocytes via the PI3-kinase-Akt pathway, the triggered signalling pathways involved in the protection of B cell from apoptosis need to be clarified. Using flow cytometry and western blot analysis, we have found that type 1 IFNs (IFN-alpha/beta) protect human B cells in culture from spontaneous apoptosis and from apoptosis mediated by anti-CD95 agonist, in a dose- and time-dependant manner. IFN-alpha/beta-mediated anti-apoptotic effect on human B cells was totally abrogated by blockade of IFNR1 chain. Our data indicate that PI3Kdelta, Rho-A, NFkappaB and Bcl-2/Bcl(XL) are active downstream of IFN receptors and are the major effectors of IFN-alpha/beta-rescued B cells from apoptosis. Furthermore, immunohistochemical results show marked reduction in numbers of CD20 positive B cell in both spleen and Peyer's patches from mice treated with anti-IFNR1 blocking antibody compared with control group. Moreover, ultrastructural observations of these organs show an obvious increase in apoptotic cells from mice treated with anti-IFNR1 blocking antibody. Our results provide more details about the triggered signalling pathways and the phosphorylation cascade which are involved in the protection of B cell from apoptosis after treatment with IFN-alpha/beta.
机译：尽管据报道IFN-α可通过PI3-激酶-Akt途径促进外周B淋巴细胞的存活，但需要阐明涉及保护B细胞免于凋亡的触发信号途径。使用流式细胞仪和蛋白质印迹分析，我们发现1型干扰素（IFN-alpha / beta）以剂量和时间依赖性方式保护培养的人B细胞免于自发凋亡和抗CD95激动剂介导的凋亡。 。 IFN-α/β介导的对人B细胞的抗凋亡作用被IFNR1链的阻滞完全消除了。我们的数据表明，PI3Kdelta，Rho-A，NFkappaB和Bcl-2 / Bcl（XL）在IFN受体的下游具有活性，并且是从凋亡中拯救出IFN-α/β的B细胞的主要作用因子。此外，免疫组化结果显示，与对照组相比，用抗IFNR1阻断抗体治疗的小鼠的脾脏和Peyer斑块中CD20阳性B细胞数量明显减少。此外，对这些器官的超微结构观察显示，用抗IFNR1阻断抗体处理的小鼠的凋亡细胞明显增加。我们的结果提供了有关触发的信号通路和磷酸化级联的更多详细信息，这些信号通路和IFN-α/β处理后可保护B细胞免于凋亡。

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