ALTERNATE IMMUNE-SYSTEM TARGETS FOR TCDD - LYMPHOCYTE STEM-CELLS AND EXTRATHYMIC T-CELL DEVELOPMENT

被引：0
|
作者：
SILVERSTONE, AE [1 ]
FRAZIER, DE [1 ]
GASIEWICZ, TA [1 ]
机构：
[1] UNIV ROCHESTER,SCH MED,CTR ENVIRONM HLTH SCI,DEPT ENVIRONM MED,ROCHESTER,NY
来源：
EXPERIMENTAL AND CLINICAL IMMUNOGENETICS | 1994年 / 11卷 / 2-3期
关键词：
APOPTOSIS; AUTOIMMUNITY; BCL-2; ONCOGENE; ESTRADIOL; DEXAMETHASONE; 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN; EXTRATHYMIC T CELLS; LYMPHOCYTE STEM CELLS; THYMIC ATROPHY;
D O I：
暂无
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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.
引用
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页码：94 / 101
页数：8
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