Cryptosporidium parvum induces B7-H1 expression in cholangiocytes by down-regulating microRNA-513.
Cryptosporidium parvum induces B7-H1 expression in cholangiocytes by down-regulating microRNA-513.
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DOI：
10.1086/648589
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发表时间：
2010-01-01
期刊：
影响因子：
--
通讯作者：
Chen XM
中科院分区：
文献类型：
--
作者：
Gong AY;Zhou R;Hu G;Liu J;Sosnowska D;Drescher KM;Dong H;Chen XM
B7共刺激分子的表达是微生物感染后上皮细胞免疫反应的重要组成部分。我们报道了原虫微小隐孢子虫诱导培养的人胆管细胞表达B7-H1。感染细小隐孢子虫或寄生虫裂解物后，B7-H1在细胞中被诱导表达。有趣的是，微小弧菌暴露后细胞中microRNA-513(miR-513)水平降低，导致3‘-非翻译区介导的B7-H1翻译抑制减轻。通过转染miR-513前体过表达miR-513可抑制微小弧菌诱导的B7-H1蛋白表达。此外，在激活的人T细胞中，与微小隐孢子虫感染的胆管细胞共培养后，证实了增强的凋亡细胞死亡。B7-H1中和抗体或miR-513前体基因转染胆管细胞可部分阻断活化T细胞的凋亡。这些数据表明miR-513在胆管细胞对微小弧菌感染的反应中调节B7-H1的表达。
Expression of B7 costimulatory molecules represents an important compartment of immune response of epithelial cells following microbial infection. We reported here that the protozoan parasite Cryptosporidium parvum induced B7-H1 expression in cultured human cholangiocytes. Induced expression of B7-H1 was identified in cells after exposure to infective C. parvum parasite or parasite lysate. Interestingly, microRNA-513 (miR-513) level was reduced in cells after exposure to C. parvum, resulting in a relief of 3′-untranslated region-mediated translational suppression of B7-H1. Overexpression of miR-513 through transfection of miR-513 precursor inhibited C. parvum-induced B7-H1 protein expression. Moreover, enhanced apoptotic cell death was identified in activated human T cells following co-culture with C. parvum-infected cholangiocytes. The apoptosis of activated T cells was partially blocked by a neutralizing antibody to B7-H1 or transfection of cholangiocytes with miR-513 precursor. These data suggest a role of miR-513 in regulating B7-H1 expression by cholangiocytes in response to C. parvum infection.
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