Academic Department of Rheumatology, Division of Immunology, Infection and Inflammatory Diseases, King's College School of Medicine, London, UK.
Trends Immunol. 2011 Jun;32(6):278-86. doi: 10.1016/j.it.2011.03.010. Epub 2011 Apr 30.
Control of IFN-γ-secreting T helper (Th) 1 cells prevents autoimmunity and immunopathology during infection. IL-10-mediated suppression of Th1 cells is achieved not only through IL-10 produced extrinsically, but also through a negative feedback loop that induces "intrinsic" IL-10 expression in cells also expressing IFN-γ, during Th1 lineage differentiation. Targeting this Th1 cell IFN-γ to IL-10 switching is a tantalising prospect for developing therapeutics for Th1-mediated diseases. In this review, the molecular pathways that regulate IFN-γ versus IL-10 expression in Th1 cells are examined, with focus on the role of complement regulator and T cell co-stimulatory molecule CD46, and also discussed are challenges and controversies in the field.
控制 IFN-γ 分泌的辅助性 T 细胞 1（Th1）细胞可预防感染期间的自身免疫和免疫病理学。IL-10 介导的 Th1 细胞抑制不仅通过外在产生的 IL-10 来实现，而且还通过在 Th1 谱系分化期间诱导同时表达 IFN-γ 的细胞中的“内在”IL-10 表达的负反馈环来实现。针对这种 Th1 细胞 IFN-γ 向 IL-10 转换的靶向治疗是开发针对 Th1 介导疾病的治疗方法的诱人前景。在这篇综述中，我们检查了调节 Th1 细胞中 IFN-γ 与 IL-10 表达的分子途径，重点关注补体调节剂和 T 细胞共刺激分子 CD46 的作用，还讨论了该领域的挑战和争议。
