Reduced tumour necrosis factor receptor superfamily 13C inversely correlated with tumour necrosis factor superfamily 13B in patients with immune thrombocytopenia

Reduced tumour necrosis factor receptor superfamily 13C inversely correlated with tumour necrosis factor superfamily 13B in patients with immune thrombocytopenia
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DOI:
10.1111/bjh.12958
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发表时间:
2014-09
影响因子:
6.5
通讯作者:
Xiao‐juan Zhu;Yan Shi;Feng Zhang;Qing-min Yao;Yan-xia Liu;Ning-ning Shan;Dan Wang;J. Peng;J. Xu;M. Hou
Xiao‐juan Zhu;Yan Shi;Feng Zhang;Qing-min Yao;Yan-xia Liu;Ning-ning Shan;Dan Wang;J. Peng;J. Xu;M. Hou
中科院分区:
医学2区
文献类型:
--
作者:
Xiao‐juan Zhu;Yan Shi;Feng Zhang;Qing-min Yao;Yan-xia Liu;Ning-ning Shan;Dan Wang;J. Peng;J. Xu;M. Hou

文献摘要

相似文献

为探讨肿瘤坏死因子超家族13 B(TNFSF 13 B)受体在免疫性血小板减少症(ITP)中的表达及其与疾病活动的相关性,我们采用流式细胞术、酶联免疫吸附试验和真实的实时定量聚合酶链反应检测了TNFSF 13 B、TNFRSF13 C、TNFRSF13 B和TNFRSF17的蛋白和mRNA水平。流式细胞术检测结果显示,所有CD 19 +B淋巴细胞均表达TNFRSF13 C,但活动期患者的平均荧光强度(MFI)较缓解期患者和健康对照组降低,而ITP患者和对照组的TNFRSF13 C mRNA表达无明显差异。活动期ITP患者TNFSF 13 C mRNA和血浆TNFSF 13 B水平升高,且TNFSF 13 C MFI水平与血浆TNFSF 13 B水平呈负相关。体外试验表明,TNFSF 13 C MFI在长时间暴露于TNFSF 13 B后降低。在ITP患者和对照组之间没有发现TNFRSF13 B或TNFRSF17的显著差异。总之,在活动性ITP患者中,CD19+细胞上TNFRSF13C表达降低。这种下调通过转录后机制发生,可能是TNFSF13 B慢性增加的结果。
To investigate the expression of tumour necrosis factor superfamily 13B (TNFSF13B) receptors in immune thrombocytopenia (ITP) and their correlation with disease activity, we investigated the protein and mRNA levels of TNFSF13B, tumour necrosis factor receptor superfamily 13C (TNFRSF13C), TNFRSF13B and TNFRSF17 by flow cytometry, enzyme‐linked immunosorbent assay and real time quantitative polymerase chain reaction. All CD19+B lymphocytes expressed TNFRSF13C by flow cytometry, but the mean fluorescence intensity (MFI) was decreased in patients with active disease compared to patients in remission and healthy controls, while no significant difference of TNFRSF13C mRNA was found between ITP patients and controls. The mRNA and plasma TNFSF13B were elevated in active ITP patients, and TNFRSF13C MFI level was inversely correlated with plasma TNFSF13B in active patients. In vitro assays showed that TNFRSF13C MFI was decreased after long exposure to TNFSF13B. No significant difference for TNFRSF13B or TNFRSF17 was found between ITP patients and controls. In conclusion, TNFRSF13C expression is reduced on CD19+ cells in active ITP patients. This down‐regulation occurs through a post‐transcriptional mechanism and could be a consequence of chronic increase of TNFSF13B.