The thymus atrophy inducing organotin compound DBTC stimulates TCRalfabeta-CD3 signalling in immature rat thymocytes

article
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 TcRαβ-CD3-complex on rat thymocytes and inhibits capping of TcRαβ. 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 Ca2+-response, suggest that DBTC interferes with TcRαβ-CD3-signalling by selective interference with cytoskeletal functioning. The responding thymocytes were CD53- and FSC(low), 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.
Chemicals/CAS: Azides; Calcium, 7440-70-2; Cytochalasin B, 14930-96-2; dibutyldichlorotin, 683-18-1; Organotin Compounds; Receptor-CD3 Complex, Antigen, T-Cell; Receptors, Antigen, T-Cell, alpha-beta; Sodium Azide, 26628-22-8; Teratogens
TNO Identifier
82719
ISSN
0006291X
Source
Biochemical and Biophysical Research Communications, 214(2), pp. 552-558.
Pages
552-558
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