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IL-10 regulates Aicda expression through miR-155

机译:IL-10通过miR-155调节Aicda表达

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摘要

Aicda is a critical component of antibody class-switching in B cells. In this work, we study the impact of TLR4 activation and IL-10 stimulation on Aicda expression in B cells. Through the global analysis of miRNAs in response to TLR4 activation, in combination with IL-10 stimulation, we identified that IL-10 can suppress TLR4-induced miR-155 expression, an effect that resulted in enhanced Aicda expression. Furthermore, when preventing miR-155 control of Aicda expression, by genetic mutation of its target site in the Aicda mRNA, IL-10 could further potentiate Aicda expression. Given that miR-155 expression is lost, and expression levels of both Aicda and IL-10 are high in diseases, such as Burkitt's lymphoma, our results suggest a stringent and sophisticated control of Aicda by a novel IL-10/miR-155 axis, where the imbalance of IL-10 and/or miR-155 may contribute to disease pathogenesis.
机译:Aicda是B细胞中抗体类别转换的关键组成部分。在这项工作中,我们研究了TLR4激活和IL-10刺激对B细胞Aicda表达的影响。通过对响应TLR4激活的miRNA进行整体分析,并结合IL-10刺激,我们发现IL-10可以抑制TLR4诱导的miR-155表达,这种作用导致Aicda表达增强。此外,当阻止miR-155控制Aicda表达时,通过在Aicda mRNA中对其靶位点进行基因突变,IL-10可以进一步增强Aicda表达。考虑到miR-155的表达丢失,并且Aicda和IL-10的表达水平在伯基特淋巴瘤等疾病中都很高,我们的研究结果表明,新型IL-10 / miR-155轴可对Aicda进行严格而精密的控制IL-10和/或miR-155的失衡可能导致疾病发病。

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