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Publication Detail

Title: Alternate immune system targets for TCDD: lymphocyte stem cells and extrathymic T-cell development.

Authors: Silverstone, A E; Frazier Jr, D E; Gasiewicz, T A

Published In Exp Clin Immunogenet, (1994)

Abstract: We here summarize evidence that thymic atrophy induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can be mediated, at least in part, by damage to extrathymic T-cell precursors in bone marrow and fetal liver. This atrophy induction does not involve apoptotic mechanisms in thymocytes affected by the bcl-2 proto-oncogene. TCDD mediates atrophy induction through its specific receptor (the AhR) and not through effects on the estrogen receptor. Both TCDD and estradiol induce extrathymic T-cell differentiation in the liver. These extrathymic T-cell populations include cells expressing elevated levels of V beta T-cell receptors that are normally deleted in thymic development.

PubMed ID: 7826670 Exiting the NIEHS site

MeSH Terms: Animals; Atrophy/chemically induced; Cell Differentiation/drug effects; Dexamethasone/toxicity; Estradiol/toxicity; Humans; Liver/drug effects; Lymphocytes/drug effects*; Polychlorinated Dibenzodioxins/toxicity*; Receptors, Aryl Hydrocarbon/drug effects; Receptors, Estradiol/drug effects; Stem Cells/drug effects; T-Lymphocytes/drug effects; Thymus Gland/cytology; Thymus Gland/drug effects*; Thymus Gland/pathology

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