Department of Microbiology, Environmental Health Sciences Center, Oregon State University, Corvallis, OR 97331, USA.
Ann N Y Acad Sci. 2010 Jan;1183:25-37. doi: 10.1111/j.1749-6632.2009.05125.x.
The immune toxicity of the ubiquitous environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), commonly referred to as dioxin, has been studied for over 35 years but only recently has the profound immune suppression induced by TCDD exposure been linked to induction of regulatory T cells (Tregs). The effects of TCDD are mediated through its binding to the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor. The subsequent AHR-dependent effects on immune responses are determined by the cell types involved, their activation status, and the type of antigenic stimulus. Collectively, studies indicate that TCDD inhibits CD4+ T cell differentiation into T helper (Th)1, Th2, and Th17 effector cells, while inducing Foxp3-negative and/or preserving Foxp3+ Tregs. Although it is not yet clear how activation of AHR by TCDD induces Tregs, there is a potential therapeutic role for alternative AHR ligands in the treatment of immune-mediated disorders.
普遍存在于环境中的污染物 2,3,7,8-四氯二苯并对二恶英（TCDD），通常被称为二恶英，其免疫毒性已被研究超过 35 年，但直到最近，TCDD 暴露所诱导的深刻免疫抑制才与调节性 T 细胞（Tregs）的诱导有关。TCDD 的作用是通过与芳烃受体（AHR）结合介导的，AHR 是一种配体激活的转录因子。随后，AHR 对免疫反应的影响取决于涉及的细胞类型、它们的激活状态和抗原刺激的类型。总的来说，研究表明，TCDD 抑制 CD4+T 细胞分化为辅助性 T 细胞（Th）1、Th2 和 Th17 效应细胞，同时诱导 Foxp3-阴性和/或保留 Foxp3+Tregs。尽管目前尚不清楚 TCDD 通过激活 AHR 如何诱导 Tregs，但替代 AHR 配体在治疗免疫介导的疾病方面具有潜在的治疗作用。
