Department of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Cell Immunol. 2011;270(2):237-50. doi: 10.1016/j.cellimm.2011.05.015. Epub 2011 May 31.
Pro-inflammatory CD4(+) T cell-mediated autoimmune diseases, such as multiple sclerosis, are hypothesized to be initiated and maintained by self-reactive interferon-gamma (IFN-γ) and interleukin-17 (IL-17) producing CD4(+) T cells. Previous studies have shown moderate to significant alterations in inflammatory T cell responses and potentially treatment of autoimmune disease by administration of antihistamine or tricyclic antidepressants alone. The goal of the present study was to determine if treatment of PLP(139-151)-induced relapsing-remitting experimental autoimmune encephalomyelitis (R-EAE) in SJL/J mice with a combination of two FDA approved drugs for other indications could decrease R-EAE disease. The findings show that combination treatment with desloratadine and nortriptyline decreases the mean clinical score, disease relapse frequency, and number of CD4(+) T cells infiltrating into the CNS. In addition, combination treatment of PLP(139-151) primed mice decreases the level of IFN-γ and IL-17 secreted via a decrease in both the number of cells secreting and the amount of cytokine secreted per cell following PLP(139-151) reactivation ex vivo. This is in contrast to an increase in the level of IL-4 produced and the number of IL-4 secreting cells. The data also show that combination treatment with desloratadine and nortriptyline inhibits the production of IFN-γ and IL-17 produced by naive CD4(+) T cells activated in the presence of Th1 cell- and Th17 cell-promoting conditions, while increasing the level of IL-4 produced by naive CD4(+) T cells activated in the presence of Th2 cell-promoting conditions. The present findings suggest a novel method for the development of a putative autoimmune therapy.
促炎性 CD4(+) T 细胞介导的自身免疫性疾病,如多发性硬化症,被假设为由自身反应性干扰素-γ (IFN-γ) 和白细胞介素-17 (IL-17) 产生的 CD4(+) T 细胞引发和维持。先前的研究表明,炎症性 T 细胞反应发生了中度至显著改变,并且通过单独给予抗组胺药或三环类抗抑郁药治疗,自身免疫性疾病可能得到潜在治疗。本研究的目的是确定是否可以用两种已批准用于其他适应证的 FDA 药物联合治疗 PLP(139-151)诱导的 SJL/J 小鼠复发缓解型实验性自身免疫性脑脊髓炎 (R-EAE),以减轻 R-EAE 疾病。研究结果表明,用地氯雷他定和去甲替林联合治疗可降低平均临床评分、疾病复发频率和浸润中枢神经系统的 CD4(+) T 细胞数量。此外,用地氯雷他定和去甲替林联合治疗 PLP(139-151) 致敏的小鼠,通过减少 PLP(139-151) 再激活后细胞分泌的细胞数量和细胞分泌的细胞因子数量,降低 IFN-γ 和 IL-17 的分泌水平。这与 IL-4 产生水平的增加和 IL-4 分泌细胞数量的增加形成对比。数据还表明,用地氯雷他定和去甲替林联合治疗抑制了在 Th1 细胞和 Th17 细胞促进条件下激活的幼稚 CD4(+) T 细胞产生的 IFN-γ 和 IL-17,同时增加了在 Th2 细胞促进条件下激活的幼稚 CD4(+) T 细胞产生的 IL-4 水平。这些发现为开发潜在的自身免疫治疗提供了一种新方法。