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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Atrophy / chemically induced
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Cell Differentiation / drug effects
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Dexamethasone / toxicity
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Estradiol / toxicity
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Humans
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Liver / drug effects
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Lymphocytes / drug effects*
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Polychlorinated Dibenzodioxins / toxicity*
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Proto-Oncogene Mas
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Receptors, Aryl Hydrocarbon / drug effects
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Receptors, Estradiol / drug effects
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Stem Cells / drug effects
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T-Lymphocytes / drug effects
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Thymus Gland / cytology
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Thymus Gland / drug effects*
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Thymus Gland / pathology
Substances
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MAS1 protein, human
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Polychlorinated Dibenzodioxins
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Proto-Oncogene Mas
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Receptors, Aryl Hydrocarbon
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Receptors, Estradiol
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Estradiol
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Dexamethasone