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Exp Clin Immunogenet. 1994;11(2-3):94-101.

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

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Department of Microbiology and Immunology, State University of New York Health Science Center, Syracuse 13210-2375.


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.

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