effects of T helper 17 and regulatory T cells on patients with carotid atherosclerosis

ABSTRACT

This study was aimed to observe the level of T helper 17 [Th17] cells and CD4[+] CD25[+] Foxp[3+] regulatory T cells [Tregs] and their related factors in carotid atherosclerosis [AS] patients and AS model rats to explore the influence of Th17 on the pathological process of AS and its specific mechanism. 60 cases with AS in our hospital from July 2012 to July 2014 were recruited for this study as the observation group, and 40 healthy people who came to the hospital for a physical examination were the control group. Flow cytometry [FCM] was used to detect the Th17 and Treg cells in the peripheral blood of the two groups, ELISA was used to detect IL-17 and transforming growth factor-beta [TGF-beta], and RTPCR was used to test the ROR gamma T mRNA and Foxp3 mRNA expression levels. An AS model was created in rats using high-fat+ VD[3] to explore the mechanism of Th17 on AS. The Th17 count, serum level of IL-17, and ROR gamma T mRNA level of the observation group were significantly higher than those of the control group [P<0.001]. The Tregs count, serum TGF-beta level, and Foxp3 mRNA level were significantly lower in the observation group than in the control group [P<0.001]. In addition, the findings of the AS model in rats showed that the Th17 cell count and serum level of IL-17 in high-fat rats were significantly higher than in the normal rats [P<0.05]. The Treg count and TGF-beta levels of the observation rats were significantly lower than in the normal rats [P<0.05]. The IL-17 level, serum total cholesterol, and triglyceride in the high-fat-feed rats decreased after being injected with the IL-17 neutralizing antibody, but TGF-beta levels increased, and the difference was significant [P<0.05]. Th17 cells and their related factors can be involved in promoting the pathological process of AS, while Tregs and its related factors can be involved in the inhibition of AS. Blocking IL-17 can be one potential method of treating AS