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首页> 外文期刊>Experimental nephrology >Regulation of Inducible Class II MHC, Costimulatory Molecules, and Cytokine Expression in TGF-beta1 Knockout Renal Epithelial Cells: Effect of Exogenous TGF-beta1.
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Regulation of Inducible Class II MHC, Costimulatory Molecules, and Cytokine Expression in TGF-beta1 Knockout Renal Epithelial Cells: Effect of Exogenous TGF-beta1.

机译：TGF-beta1敲除肾上皮细胞中诱导性II类MHC，共刺激分子和细胞因子表达的调节：外源TGF-beta1的影响。

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摘要

As reports of mice genetically deficient for TGF-beta1 demonstrated aberrant renal class II MHC expression, we investigated inducible class II MHC expression on renal tubular epithelial cells derived from TGF-beta1 knockout (-/-) and wild-type (+/+) mice. IFN-gamma markedly upregulated class II MHC (I-A(b)) expression in both (-/-) and (+/+) tubular epithelial cells. Coincubation studies of (+/+) and (-/-) tubular epithelial cells with IFN-gamma+LPS, or pretreatment of these cells with TGF-beta1, revealed inhibition of IFN-gamma-induced I-A(b) mRNA and cell surface expression that occurred via a decrease in class II transactivator gene expression in both (+/+) and (-/-) tubular epithelial cells. In addition, ICAM-1 was constitutively expressed on both (+/+) and (-/-) tubular epithelial cells and was upregulated by IFN-gamma or IFN-gamma+LPS. ICAM-1 expression in (+/+) and (-/-) tubular epithelial cells, however, was decreased by TGF-beta1. Parallel analysis evaluating B7-1 expression detected low levels of B7-1 in unstimulated (+/+) and (-/-) tubular epithelial cells that were increased by IFN-gamma, LPS, and IFN-gamma+LPS. IFN-gamma+LPS-mediated upregulation of B7-1 was also blocked by pretreatment with TGF-beta1. Cytokine analysis detected significantly higher levels of TNF-alpha and MIP-1alpha mRNA in all treated (-/-) preparations than in (+/+) tubular epithelial cell controls. These studies demonstrate normal patterns of class II MHC, ICAM-1, and B7 expression in TGF-beta1 (-/-) tubular epithelial cells in response to IFN-gamma, LPS, and TGF-beta1. Upregulated cytokine expression at baseline and in response to proinflammatory mediators is apparent in (-/-) tubular epithelial cells, however, and suggests that dysregulation of cytokine expression in inflammatory responses may be a primary event in multifocal inflammation observed in TGF-beta1-deficient animals. Copyright 2002 S. Karger AG, Basel
机译：由于对TGF-beta1遗传缺陷的小鼠的报告显示了异常的II类肾MHC表达，我们研究了从TGF-beta1敲除（-/-）和野生型（+ / +）衍生的肾小管上皮细胞上诱导型II MHC表达老鼠。 IFN-γ显着上调了（-/-）和（+ / +）肾小管上皮细胞中的II类MHC（I-A（b））表达。 （+ / +）和（-/-）肾小管上皮细胞与IFN-γ+ LPS的共孵育研究，或用TGF-beta1预处理这些细胞，发现抑制了IFN-γ诱导的IA（b）mRNA和细胞表面在（+ / +）和（-/-）肾小管上皮细胞中通过II类反式激活基因表达的降低而引起的蛋白表达。另外，ICAM-1在（+ / +）和（-/-）肾小管上皮细胞上组成性表达，并被IFN-γ或IFN-γ+ LPS上调。 TGF-beta1降低了（+ / +）和（-/-）肾小管上皮细胞中的ICAM-1表达。评估B7-1表达的平行分析在未刺激的（+ / +）和（-/-）肾小管上皮细胞中检测到低水平的B7-1，这些水平被IFN-γ，LPS和IFN-γ+ LPS增加。 TGF-beta1预处理也可以阻断IFN-γ+ LPS介导的B7-1的上调。细胞因子分析检测到，在所有处理过的（-/-）制剂中，TNF-α和MIP-1alpha mRNA的含量均显着高于（+ / +）管状上皮细胞对照。这些研究表明响应IFN-γ，LPS和TGF-beta1，TGF-beta1（-/-）肾小管上皮细胞中II类MHC，ICAM-1和B7表达的正常模式。在（-/-）肾小管上皮细胞中明显出现了基线和对促炎介质反应的细胞因子表达上调，但是，这表明在炎症反应中细胞因子表达失调可能是在TGF-β1缺陷型多灶性炎症中发生的主要事件。动物。版权所有2002 S. Karger AG，巴塞尔

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