Abstract
Helper T cell 17 (Th17) being a new cell subset of CD4+T in the body, which is different from Th1 and Th2 cells, have independent mechanisms of differentiation and developmental regulation. Th17 cells mainly secrete various cytokines such as IL-17, IL-6 and TNF-α, which induce inflammation. Treg cells are T cells with high expression of CD25 differentiated by T cells under the action of certain cytokines, namely CD4+CD25+(hi) Foxp3+T cells, which can regulate the immune response mediated by effector cells and are an important line of defense for human autoimmune. Therefore, Treg cells play an important role in maintaining immune tolerance of the body. As an important subset of T cells, Treg cells have an inhibitory effect on inflammation. Its working principle is to selectively inhibit autoreactive T cells and effector T cells so as to maintain the body's immune balance, and normal quantity and function help the immune system to its antigen stimulation, establishing a good state of tolerance. The expression of Treg cells increased, can avoid the occurrence of autoimmune diseases. Treg cells inhibit the differentiation of Th17 cells by down-regulating the expression of IL-23 and IL-17 or by its specific transcription factor Foxp3; similarly, inhibition of Th17 cell production can promote the development of Treg cells. Both Th17 and Treg cells are functionally inhibited. Th17 cells promote inflammatory reaction, and Treg cells suppress immune reaction. Numerous cytokines are involved in regulation. For example, IL-6 and IL-21 can inhibit Foxp3 and promote the expression of RORγt, thereby inhibiting Treg cells and inducing the differentiation of Th17 cells. In the absence of IL-6 and other pro-inflammatory factors, TGF-β enhances the inhibitory effect of Foxp3 on RORγt and promotes the growth and development of Treg cells. The anti-inflammatory factor IL-10 also induces Treg cells to inhibit the reaction of Th17 cells. The effects of Treg and Th17 cells are normally in a dynamic equilibrium. Once the balance is imbalanced, autoimmune diseases will occur. This article reviews the differentiation, function and research progress of Th17/Treg cells in autoimmune diseases.
Highlights
Th17 cells are a new type of effector CD4+T cells subset that is different from Th1 and Th2 cells
Th17 cell are a new type of effector CD4+T cells subset which is different from Th1 and Th2 cells, characterized by specific secretion of high levels of interleukin 17(il-17) [5]
Zhao et al [87] reported that interleukin 17 (IL-17)+lymphocyte infiltration was significantly increased in patients with Autoimmune hepatitis (AIH), and the degree of infiltration was positively correlated with the degree of inflammation and abnormality of AIH, and Th17 cells and serum IL-17 were significantly higher than the control group, which indicated that Th17 cell proliferation played a key role in the pathogenesis of AIH
Summary
Th17 cells are a new type of effector CD4+T cells subset that is different from Th1 and Th2 cells. As a kind of immunosuppressive T cell, regulatory T cell (Treg) plays an antagonistic role with Thl cells and plays a regulatory role in immune inflammatory response, which is a key factor to maintain peripheral immune tolerance [2]. The TGF-β signaling pathway plays an important role in the differentiation of Th17 and Zhenjiang Hou et al.: Research Progress of Th17/Treg Cells and Their Transcription Factors in Autoimmune Diseases. The balance of th and Treg cells plays an important role in autoimmune tolerance and immune homeostasis, and has become the research direction of the occurrence, development and prognosis of immune-related diseases. Th17 cell and its secreted IL-17 expression and dysfunction are closely related to the development of autoimmune diseases. The increased expression of Treg cells avoids the occurrence of autoimmune diseases
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: American Journal of Clinical and Experimental Medicine
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
