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首页> 外文期刊>Cytokine >Mechanisms of CD26/dipeptidyl peptidase IV cytokine-dependent regulation on human activated lymphocytes.
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Mechanisms of CD26/dipeptidyl peptidase IV cytokine-dependent regulation on human activated lymphocytes.

机译：CD26 /二肽基肽酶IV对人活化淋巴细胞的细胞因子依赖性调节机制。

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Among the cellular pathways activated by IL-12, we had previously found that both the percentage and intensity of CD26(+)cells in the PHA-stimulated T cells increased when IL-12 was present (independently of its CD4 or CD8 phenotype). Now, we examined the molecular mechanisms of this IL-12-mediated effect. The IL-12 regulation pathway is dependent of de novo protein synthesis and independent of cytokine secretion. Our results show two transcripts for CD26 in PBMC for the first time and no regulation by ILs at this level. Furthermore, secretion of the serum forms of CD26/DPPIV were not affected by IL-12. Interestingly, assays with neutralizing mAbs against TNF-alpha suggest that this cytokine negatively modulates CD26 expression. The fact that translation and probably translocation of CD26 toward the cell surface can be regulated by IL-12 and TNF-alpha reveals new aspects about the control of this T(H1)marker. Copyright 2000 Academic Press.
机译：在IL-12激活的细胞途径中，我们先前发现当IL-12存在时，PHA刺激的T细胞中CD26（+）细胞的百分比和强度都会增加（独立于其CD4或CD8表型）。现在，我们研究了这种IL-12介导的作用的分子机制。 IL-12调节途径依赖于从头蛋白合成，并且不依赖于细胞因子的分泌。我们的结果首次显示了PBMC中CD26的两个转录本，并且在该水平上不受IL调节。此外，IL-12不会影响血清形式的CD26 / DPPIV的分泌。有趣的是，用针对TNF-α的中和mAb的测定表明该细胞因子负调节CD26的表达。 IL-12和TNF-α可以调节CD26向细胞表面的转移以及可能向细胞表面的转移，这一事实揭示了有关控制T（H1）标记的新方面。版权所有2000学术出版社。

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