Abstract
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.
Highlights
Inflammatory bowel disease (IBD) is a chronic idiopathic inflammatory disease of the digestive tract, including Crohn’s disease (CD) and ulcerative colitis (UC)
These results indicate that T helper cell 17 (Th17) and Treg are closely related to inflammatory bowel disease, and there may be an antagonistic relationship; patients with IBD exhibit reduced numbers of peripheral Treg cells, and increased numbers of peripheral Th17 cells corroborated this [28]
Recent studies have demonstrated that Foxp3+ Treg cells express retinoic acid receptor-related orphan receptor gamma t and are able to differentiate into Th17 cells, a process that is associated with a decreased suppressive Treg cell function in patients with IBD
Summary
Inflammatory bowel disease (IBD) is a chronic idiopathic inflammatory disease of the digestive tract, including Crohn’s disease (CD) and ulcerative colitis (UC). Their clinical manifestations have common characteristics, such as diarrhea, abdominal pain, and bloody stools. Th17 is a helper T cell differentiated from naive T cells under the stimulation of IL6 and IL23 It mainly secretes proinflammatory factors such as IL17 and IL22 and plays an important role in inflammatory diseases. With more in-depth research on Th17 cells, people have found that Th17 cells are at the core of autoimmune diseases (especially IBD) Since it was discovered in 2005, Th17 cells have been strongly associated with the pathogenesis of IBD [8]. This article reviews many previous studies on Th17 and IBD, aiming to clarify the influence of Th17 from differentiation to pathogenesis on IBD and try to bring new ideas to researchers in the immunotherapy of IBD
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