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Analysis of the cDNA sequence encoding MHC-A[beta] in tubular epithelium from mouse kidney

机译:小鼠肾小管上皮中编码MHC-Aβ的cDNA序列的分析

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Analysis of the cDNA sequence encoding MHC-A in tubular epithelium from mouse kidney. Class II gene products of the major histocompatibility complex (MHC) are not expressed usually in abundance on normal epithelium. The cell surface visibility of such proteins for the immune system is thought to be limited protectively in order to minimize inflammation consequent to the recognition of self-antigens in parenchymal structures by T lymphocytes. In the current experiments we investigated whether the previously recognized sparseness of A on the surface of tubular epithelial cells might be accounted for by a protein coding difference deduced from the primary structure of its transcript compared with sequence from lymphoid cells that normally express A in generous amounts. We demonstrate, however, using clones obtained from a cDNA library prepared from tubular epithelium harvested from H-2S (A/+E/-) mice susceptible to autoimmune interestitial nephritis, that the nucleotide sequence encoding the class II A chain in cells from both compartments is essentially identical. Our findings suggest that there is no primary structural aberrancy in the coding region of parenchymal A that would contribute to its low expression. The protective tolerance afforded by reduced numbers of class II molecules in normal tissues is, therefore, more likely the result of repressive regulatory processes.
机译:小鼠肾小管上皮中编码MHC-A的cDNA序列分析。主要组织相容性复合物(MHC)的II类基因产物通常不会在正常上皮中大量表达。认为这种蛋白质对免疫系统的细胞表面可见性受到保护性限制,以最小化由于T淋巴细胞识别实质结构中自身抗原而导致的炎症。在当前的实验中,我们调查了先前公认的肾小管上皮细胞表面稀疏性是否可能是由于其转录物一级结构与通常大量表达A的淋巴样细胞的序列相比较而导致的蛋白质编码差异造成的。 。但是,我们证明了使用从cDNA库中获得的克隆,该cDNA库是从对自身免疫性兴趣性肾炎敏感的H-2S(A / + E /-)小鼠收获的肾小管上皮制备的,该核苷酸序列编码两种细胞中的II A类链隔间本质上是相同的。我们的发现表明,在实质A的编码区中不存在会导致其低表达的主要结构异常。因此,正常组织中减少的II类分子数量提供的保护性耐受更有可能是抑制性调节过程的结果。

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