Association Between IL-17A, FOXP3, and CTLA4 Genes Expression and Severity of Lupus Nephritis

Abstract

Introduction. Elevated levels of interleukin 17A (IL-17A) have been found in systemic lupus erythematosus (SLE). Forkhead box protein P3 (FOXP3) activates T-regulation lymphocytes and is a master regulator cell function. The cytotoxic T-lymphocyte-associated protein 4 (CTLA4) gene plays a similar role. We investigated the role of these expressions in SLE patients with/without nephritis. Methods. The present study was a case-controlled study including 49 patients with SLE and 26 healthy controls. The genes expression of IL-17A, FOXP3, and CTLA4 were measured by quantitative Real-Time PCR. The relation between lupus nephritis and disease activity with IL-17A, FOXP3, and CTLA4 genes expression was evaluated. Results. IL-17A, FOXP3, and CTLA4 expressions in T-cells were significantly higher in SLE patients than controls (P < .0001). When comparing the nephritis group and no nephritis group to the control group individually, the expression of mentioned genes is also higher (P < .05). There was no significant difference regarding IL-17A, FOXP3, and CTLA4 genes expression in the nephritis group and no nephritis group (P > .05). But there was a low expression of FOXP3 and IL-17A in patients with the higher stage of nephritis (P < .05). Conclusion. Our findings elevated IL-17A, FOXP3, and CTLA4 expressions significantly contribute to SLE pathophysiology. This study provides new insight into the function of IL-17A, FOXP3, and CTLA4 in disease setting. The heterogeneity of SLE patients is reflected in the multiple abnormalities found in the immune system. Finding such variations can provide targets for better manipulation of the immune system.

DOI: 10.52547/ijkd.6537