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诱导胸腺萎缩的有机锡化合物二丁基锡二氯化物刺激未成熟大鼠胸腺细胞中的TcRαβ-CD3信号传导。

The thymus atrophy inducing organotin compound DBTC stimulates TcR alpha beta-CD3 signalling in immature rat thymocytes.

作者信息

Pieters R H, Punt P, Bol M, van Dijken J M, Seinen W, Penninks A H

机构信息

Research Institute of Toxicology, Utrecht University, The Netherlands.

出版信息

Biochem Biophys Res Commun. 1995 Sep 14;214(2):552-8. doi: 10.1006/bbrc.1995.2321.

Abstract

In the present study, we show that the thymus atrophy inducing compound DBTC stimulates the intracellular release, but not the influx, of Ca2+ elicited by cross-linking of the TcR alpha beta-CD3-complex on rat thymocytes and inhibits capping of TcR alpha beta. Similarities with the effects of cytochalasin B together with the finding that DBTC also inhibited capping of CD8, whereas cross-linking of CD8 did not cause a Ca(2+)-response, suggest that DBTC interferes with TcR alpha beta-CD3-signalling by selective interference with cytoskeletal functioning. The responding thymocytes were CD53- and FSClow, thus possibly including the non proliferating counterpart of the presumed immature CD4-CD8+CD53-target cells of DBTC. The present effects may therefore relate to the mechanisms of organotin-induced thymus atrophy.

摘要

在本研究中,我们发现诱导胸腺萎缩的化合物二丁基锡化合物(DBTC)可刺激大鼠胸腺细胞上T细胞受体αβ-CD3复合物交联引发的Ca2+胞内释放,但不影响其流入,并抑制T细胞受体αβ的帽化。与细胞松弛素B的作用相似,以及DBTC也抑制CD8帽化的发现,而CD8交联不会引起Ca(2+)反应,表明DBTC通过选择性干扰细胞骨架功能来干扰T细胞受体αβ-CD3信号传导。反应性胸腺细胞为CD53-和FSClow,因此可能包括DBTC假定的未成熟CD4-CD8+CD53靶细胞的非增殖对应物。因此,目前的效应可能与有机锡诱导胸腺萎缩的机制有关。

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