The thymus atrophy-inducing organotin compound dbtc inhibits the binding of thymocytes to thymic epithelial cells

Raymond H.H. Pieters, Ruud Albers, Rob Bleumink, Niek J. Snoeij, Tsunetoshi Itoh, Willem Seinen, Andr ÉH Penninks

研究成果: Article査読

8 被引用数 (Scopus)

抄録

In this study, it is examined whether the organotin compound di-n-butyltindichloride (DBTC), which has been shown to inhibit immature thymocyte proliferation, is able to disturb the binding between thymocytes and thymic epithelial cells (TEC). To that end, an enzyme-linked binding assay was developed in which the amount of binding of Thy-1+ (mAb ER4)-thymocytes to the rat-derived TEC-line IT45R1 (IT45R1-TEC) could be detected. It was found that preincubation of thymocytes with 3-5 μM DBTC for 30 min inhibited the binding by 50-60% during a 1 h adhesion period. By extending the preincubation period to 1 h and the adhesion period to 22 h, 0.1 μM DBTC was already sufficient to reduce the binding with 60-80%. Further characterization of the binding revealed that splenic lymphocytes were unable to bind to the MHC class II-negative IT45R1-TEC. Since dextran sulfate inhibited the binding as well, sulfated polysaccharide-binding molecules such as Thy-I and CD2 are likely to be involved in the binding. Electron microscopy showed filament-containing microvilli at the site of interaction. The results are discussed in relation to the mechanism of DBTC-induced thymus atrophy.

本文言語English
ページ(範囲)329-333,335-337
ジャーナルInternational Journal of Immunopharmacology
17
4
DOI
出版ステータスPublished - 1995 4

ASJC Scopus subject areas

  • 免疫学
  • 薬理学

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