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下调长链非编码 RNA 2900052N01Rik 可抑制 LPS 诱导的体外 B 细胞功能。

Down-regulation of LncRNA 2900052N01Rik inhibits LPS-induced B cell function in vitro.

机构信息

Department of Biochemistry and Molecular Biology, Medical School of Southeast University, # 87 Dingjiaqiao Road, Nanjing 210009, China.

Department of Biochemistry and Molecular Biology, Medical School of Southeast University, # 87 Dingjiaqiao Road, Nanjing 210009, China; Key Laboratory for Developmental Genes and Human Disease, Ministry of Education, Institute of Life Sciences, Southeast University, Nanjing 210096, China.

出版信息

Cell Immunol. 2021 May;363:104321. doi: 10.1016/j.cellimm.2021.104321. Epub 2021 Mar 6.

DOI:10.1016/j.cellimm.2021.104321
PMID:33773377
Abstract

B cells play a crucial role in immune responses. The main functions include B cell protective antibody production, inflammation reduction, activation and proliferation. Long non-coding RNAs (lncRNAs) have been reported to act as important regulators of many pathological processes. However, few lncRNAs have been reported to affect B cell function. In this study, we explored the expression and role of lncRNA 2900052N01Rik (lnc-290) in lipopolysaccharide (LPS)-induced B cells purified from mouse spleens in vitro. Here, we confirmed that lnc-290 was highly expressed in B cells stimulated by LPS. Knockdown of lnc-290 inhibited the expression of CD69/CD86 and the growth of B cells. Moreover, down-regulated lnc-290 reduced B cell differentiation and immunoglobulin production in vitro. In addition, we found that lnc-290 regulated LPS-induced B cell activation via the NF-κB/ERK pathways. Interestingly, abnormal lnc-290 expression did not alter the B cell activation or proliferation induced by IL-4 or CD40/CD40L. Accordingly, these results indicated, for the first time, that lnc-290 down-regulation inhibits LPS-induced B cell proliferation, activation and differentiation by blocking the LPS/TLR4 signaling pathway. Together, the in vitro data demonstrate that lnc-290 participated in the inflammation and tissue damage mediated by LPS-activated B cells.

摘要

B 细胞在免疫反应中发挥着至关重要的作用。其主要功能包括 B 细胞保护性抗体的产生、炎症的减轻、激活和增殖。长链非编码 RNA(lncRNA)已被报道作为许多病理过程的重要调节因子。然而,很少有 lncRNA 被报道影响 B 细胞功能。在本研究中,我们探讨了 lncRNA 2900052N01Rik(lnc-290)在体外 LPS 诱导的小鼠脾脏 B 细胞中的表达和作用。在这里,我们证实 lnc-290 在 LPS 刺激的 B 细胞中高表达。lnc-290 的敲低抑制了 CD69/CD86 的表达和 B 细胞的生长。此外,下调 lnc-290 减少了体外 B 细胞的分化和免疫球蛋白的产生。此外,我们发现 lnc-290 通过 NF-κB/ERK 通路调节 LPS 诱导的 B 细胞激活。有趣的是,异常的 lnc-290 表达并不改变 IL-4 或 CD40/CD40L 诱导的 B 细胞激活或增殖。因此,这些结果首次表明,lnc-290 通过阻断 LPS/TLR4 信号通路下调抑制 LPS 诱导的 B 细胞增殖、激活和分化。总之,体外数据表明,lnc-290 参与了 LPS 激活的 B 细胞介导的炎症和组织损伤。

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