Infection Immunology, Research Centre Borstel, D-23845 Borstel, Germany.
Core Facility Fluorescence Cytometry, Research Centre Borstel, D-23845 Borstel, Germany.
Cells. 2020 Dec 22;10(1):9. doi: 10.3390/cells10010009.
Anti-inflammatory treatment of chronic inflammatory diseases often increases susceptibility to infectious diseases such as tuberculosis (TB). Since numerous chronic inflammatory and autoimmune diseases are mediated by interleukin (IL)-6-induced T helper (TH) 17 cells, a TH17-directed anti-inflammatory therapy may be preferable to an IL-12-dependent TH1 inhibition in order to avoid reactivation of latent infections. To assess, however, the risk of inhibition of IL-6-dependent TH17-mediated inflammation, we examined the TH17 immune response and the course of experimental TB in IL-6- and T-cell-specific gp130-deficient mice. Our study revealed that the absence of IL-6 or gp130 on T cells has only a minor effect on the development of antigen-specific TH1 and TH17 cells. Importantly, these gene-deficient mice were as capable as wild type mice to control mycobacterial infection. Together, in contrast to its key function for TH17 development in other inflammatory diseases, IL-6 plays an inferior role for the generation of TH17 immune responses during experimental TB.
慢性炎症性疾病的抗炎治疗常常会增加感染结核病（TB）等传染病的易感性。由于许多慢性炎症和自身免疫性疾病是由白细胞介素（IL）-6 诱导的辅助性 T 细胞（TH）17 细胞介导的，因此针对 TH17 的抗炎治疗可能优于依赖 IL-12 的 TH1 抑制，以避免潜伏感染的再激活。然而，为了评估抑制 IL-6 依赖性 TH17 介导的炎症的风险，我们研究了 IL-6 和 T 细胞特异性 gp130 缺陷小鼠中的 TH17 免疫反应和实验性 TB 的病程。我们的研究表明，T 细胞缺乏 IL-6 或 gp130 对抗原特异性 TH1 和 TH17 细胞的发育仅有轻微影响。重要的是，这些基因缺陷小鼠与野生型小鼠一样能够控制分枝杆菌感染。总之，与 IL-6 在其他炎症性疾病中对 TH17 发育的关键作用相反，在实验性 TB 期间，IL-6 对 TH17 免疫反应的产生仅发挥次要作用。
