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

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 of cell function. The cytotoxic T-lymphocyte-associated protein 4 (CTLA4) gene plays a similar role. We investigated the role of the expression of these genes in SLE patients with and without nephritis.

The present study was a case-controlled trial including 49 patients with SLE and 26 healthy controls. Gene expressions of IL-17A, FOXP3, and CTLA4 were measured by quantitative Real- Time PCR. The relation between lupus nephritis disease activity and IL-17A, FOXP3, and CTLA4 gene expression was evaluated.

IL-17A, FOXP3, and CTLA4 expression in T-cells were significantly higher in SLE patients than controls (P< .0001). When comparing the nephritis group and non- nephritis group with the control group, the expression of the mentioned genes was also higher (P < .05). There was no significant difference regarding IL- 17A, FOXP3, and CTLA4 genes expression in the nephritis group and non- nephritis group (P > .05). Nonetheless, there was a low expression of FOXP3 and IL-17A in patients with the higher stages of nephritis (P < .05).

Our findings showed that elevated IL-17A, FOXP3, and CTLA4 expression significantly correlate with SLE pathophysiology. This study provides new insight into the function of IL-17A, FOXP3, and CTLA4 in a disease setting. 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.