Pieters R H, Punt P, Bol M, van Dijken J M, Seinen W, Penninks A H
Research Institute of Toxicology, Utrecht University, The Netherlands.
Biochem Biophys Res Commun. 1995 Sep 14;214(2):552-8. doi: 10.1006/bbrc.1995.2321.
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.
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。
