Abstract
The incidence of rheumatoid arthritis (RA) has been reported to be correlated with a disorder of immunregulation. Rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs) play an important role in regulating the local immune microenvironment. However, the potential mechanism of RA-FLS in regulating the immnue response is not clearly understood. In this study, we demonstrated that the expression of HIF-1α was significantly up-regulated in rheumatoid arthritis tissue which indicated that the hypoxia condition in the microenvironment. We also observed that RA-FLSs demonstrated the potential to up-regulate immune activation. Meanwhile, the level of autophagy increased in RA-FLSs compared with control group. Besides that, the expression of IL-6 was up-regulated not only in RA-FLSs but also in the fibroblasts that treated with hypoxia condition. Accordingly, we found that autophagy inhibitiors could effectively inhibit the immune activation function of RA-FLSs medicated by IL-6. Taken together, the results we demonstrated above indicated that the hypoxia microenvironment could effectively induce the incidence of autophagy and then lead to the immune activation function of RA-FLSs medicated by IL-6.
Highlights
Rheumatoid arthritis (RA) is an autoimmunemediated chronic inflammatory joint disease which affects approximately 1% of the population with disability and decreased quality of life in the end-stage [1, 2]
We demonstrated that the expression of HIF-1α was significantly up-regulated in rheumatoid arthritis tissue which indicated that the hypoxia condition in the microenvironment
The results we demonstrated above indicated that the hypoxia microenvironment could effectively induce the incidence of autophagy and lead to the immune activation function of rheumatoid arthritis (RA)-Fibroblast-like synoviocytes (FLS) medicated by IL-6
Summary
Rheumatoid arthritis (RA) is an autoimmunemediated chronic inflammatory joint disease which affects approximately 1% of the population with disability and decreased quality of life in the end-stage [1, 2]. Many investigations have indicated that RA is caused by genetic and/or environmental factors and characteristically affect the small joints of the hands and feet which often lead to joint structure destruction and functional impairment [3, 4]. Increased studies demonstrated the pathogenetic mechanism of RA was caused by cytokine networks and associated cells [5]. Inhibition of inflammation may not be sufficient to suppress the progression of RA and the mechanisms of RA need further exploring
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