Autoimmune diseases (such as rheumatoid arthritis, asthma, autoimmune bowel disease) are a complex disease. Improper activation of the immune system or imbalance of immune cells can cause the immune system to transform into a proinflammatory state, leading to autoimmune pathological damage. Recent studies have shown that autoimmune diseases are closely related to CD4+ T helper cells (Th). The original CD4 T cells will differentiate into different T helper (Th) subgroups after activation. According to their cytokines, the types of Th cells are different to produce lineage-specific cytokines, which play a role in autoimmune homeostasis. When Th differentiation and its cytokines are not regulated, it will induce autoimmune inflammation. Autoimmune bowel disease (IBD) is an autoimmune disease of unknown cause. Current research shows that its pathogenesis is closely related to Th17 cells. This article reviews the role and plasticity of the upstream and downstream cytokines and signaling pathways of Th17 cells in the occurrence and development of autoimmune bowel disease and summarizes the new progress of IBD immunotherapy.

中文翻译：

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炎症性肠病中的 Th17 细胞：细胞因子、可塑性和治疗

自身免疫性疾病（如类风湿性关节炎、哮喘、自身免疫性肠病）是一种复杂的疾病。免疫系统的不当激活或免疫细胞的失衡都会导致免疫系统转变为促炎状态，导致自身免疫病理损伤。最近的研究表明，自身免疫性疾病与 CD4+ T 辅助细胞 (Th) 密切相关。原始 CD4 T 细胞在激活后会分化为不同的 T 辅助 (Th) 亚群。根据它们的细胞因子，不同类型的 Th 细胞产生谱系特异性细胞因子，在自身免疫稳态中发挥作用。当 Th 分化及其细胞因子不受调控时，会诱发自身免疫性炎症。自身免疫性肠病（IBD）是一种原因不明的自身免疫性疾病。目前研究表明其发病机制与Th17细胞密切相关。本文综述了Th17细胞上下游细胞因子和信号通路在自身免疫性肠病发生发展中的作用和可塑性，总结了IBD免疫治疗的新进展。