Long Carrie Mae, Marshall Nikki B, Lukomska Ewa, Kashon Michael L, Meade B Jean, Shane Hillary, Anderson Stacey E
*Allergy and Clinical Immunology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, West Virginia 26505 Immunology and Microbial Pathogenesis Graduate Program, West Virginia University School of Medicine, Morgantown, West Virginia 26505
*Allergy and Clinical Immunology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, West Virginia 26505.
Toxicol Sci. 2016 Jul;152(1):85-98. doi: 10.1093/toxsci/kfw074. Epub 2016 Apr 21.
Toluene diisocyanate (TDI) is a leading cause of chemical-induced occupational asthma which impacts workers in a variety of industries worldwide. Recently, the robust regulatory potential of regulatory T cells (Tregs) has become apparent, including their functional role in the regulation of allergic disease; however, their function in TDI-induced sensitization has not been explored. To elucidate the kinetics, phenotype, and function of Tregs during TDI sensitization, BALB/c mice were dermally exposed (on each ear) to a single application of TDI (0.5-4% v/v) or acetone vehicle and endpoints were evaluated via RT-PCR and flow cytometry. The draining lymph node (dLN) Treg population expanded significantly 4, 7, and 9 days after single 4% TDI exposure. This population was identified using a variety of surface and intracellular markers and was found to be phenotypically heterogeneous based on increased expression of markers including CD103, CCR6, CTLA4, ICOS, and Neuropilin-1 during TDI sensitization. Tregs isolated from TDI-sensitized mice were significantly more suppressive compared with their control counterparts, further supporting a functional role for Tregs during TDI sensitization. Last, Tregs were depleted prior to TDI sensitization and an intensified sensitization response was observed. Collectively, these data indicate that Tregs exhibit a functional role during TDI sensitization. Because the role of Tregs in TDI sensitization has not been previously elucidated, these data contribute to the understanding of the immunologic mechanisms of chemical induced allergic disease.
甲苯二异氰酸酯(TDI)是化学诱导职业性哮喘的主要病因,影响着全球各行各业的工人。最近,调节性T细胞(Tregs)强大的调节潜力已变得明显,包括它们在过敏性疾病调节中的功能作用;然而,它们在TDI诱导致敏中的功能尚未得到探索。为了阐明TDI致敏过程中Tregs的动力学、表型和功能,将BALB/c小鼠(每只耳朵)经皮单次暴露于TDI(0.5-4% v/v)或丙酮载体,通过逆转录聚合酶链反应(RT-PCR)和流式细胞术评估终点指标。单次暴露于4% TDI后4天、7天和9天,引流淋巴结(dLN)中的Treg群体显著扩大。使用多种表面和细胞内标志物鉴定了该群体,发现其在TDI致敏期间基于包括CD103、CCR6、CTLA4、ICOS和神经纤毛蛋白-1等标志物表达增加而表现出表型异质性。与对照小鼠相比,从TDI致敏小鼠中分离出的Tregs具有显著更强的抑制作用,进一步支持了Tregs在TDI致敏过程中的功能作用。最后,在TDI致敏前耗尽Tregs,观察到致敏反应增强。总体而言,这些数据表明Tregs在TDI致敏过程中发挥功能作用。由于Tregs在TDI致敏中的作用此前尚未阐明,这些数据有助于理解化学诱导过敏性疾病的免疫机制。