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

页码：94 / 101

页数：8