抑制肿瘤坏死因子活性无法恢复2,3,7,8-四氯二苯并对二恶英（TCDD）诱导的对绵羊红细胞抗体反应的抑制。

Inhibition of tumor necrosis factor activity fails to restore 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced suppression of the antibody response to sheep red blood cells.

作者信息

Moos A B, Kerkvliet N I

机构信息

College of Veterinary Medicine, Oregon State University, Corvallis 97331-7304, USA.

出版信息

Toxicol Lett. 1995 Nov 15;81(2-3):175-81. doi: 10.1016/0378-4274(95)03429-3.

DOI:10.1016/0378-4274(95)03429-3

PMID:8553372

Abstract

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) immunotoxicity is characterized in part by a profound suppression in T cell-dependent antibody production to sheep red blood cells (SRBC); however the mechanisms involved in antibody suppression are not fully understood. Recent studies from several different laboratories have suggested that increased tumor necrosis factor (TNF) activity may mediate some of the toxicity associated with TCDD exposure. The current studies were designed to evaluate the role TNF plays in TCDD-induced suppression of the antibody response. We examined the effects of exogenous TNF alpha and the effects of blocking TNF activity with a soluble TNF receptor (rhuTNFR:Fc) on antibody production in control and TCDD exposed C57B1/6 mice. Results indicate that under certain conditions, increased TNF can suppress antibody production to SRBC, but TNF does not appear to mediate TCDD-induced antibody suppression.

摘要

2,3,7,8-四氯二苯并-对-二噁英（TCDD）的免疫毒性部分表现为对绵羊红细胞（SRBC）的T细胞依赖性抗体产生的显著抑制；然而，抗体抑制所涉及的机制尚未完全明确。来自几个不同实验室的近期研究表明，肿瘤坏死因子（TNF）活性增加可能介导了与TCDD暴露相关的一些毒性。当前的研究旨在评估TNF在TCDD诱导的抗体反应抑制中所起的作用。我们检测了外源性TNFα的作用以及用可溶性TNF受体（rhuTNFR:Fc）阻断TNF活性对对照和TCDD暴露的C57B1/6小鼠抗体产生的影响。结果表明，在某些条件下，TNF增加可抑制对SRBC的抗体产生，但TNF似乎并未介导TCDD诱导的抗体抑制。