Increased Macroautophagy in Interferon-Gamma-Producing T Cells from Patients with Newly Diagnosed Systemic Lupus Erythematosus.

Background: Imbalance of interferon-gamma (IFN-gamma), interleukin (IL)-4, and IL-17 producing by T cells is confirmed to contribute to the pathogenesis of systemic lupus erythematosus (SLE). Autophagy is now emerging as a core player in the development and the function of the immune system. Therefore, we investigated the autophagic behavior in IFN-gamma-, IL-4-, and IL-17-producing T cells from patients with SLE. Methods: Thirty patients with SLE and 25 healthy controls matched for gender and age were recruited between September 2016 and May 2017. The autophagic levels in IFN-gamma(+) T cells, IL-4(+) T cells, and IL-17(+) T cells from patients with newly diagnosed SLE and healthy controls were measured using flow cytometry. The plasma levels of IFN-gamma were determined by enzyme- linked immunosorbent assay in SLE patients and healthy controls. Unpaired ittests and the nonparametric Mann-Whitney U-test were used to compare data from patients with SLE and controls. Spearman's rank correlation coefficient was applied for calculation of the correlation between parallel variables in single samples. Results: Our results showed increased percentage of autophagy in IFN-gamma(+) T cells from patients with SLE and healthy controls ([8.07 +/- 2.72]% vs. [3.76 +/- 1.67]%, t = 5.184, P < 0.001), but not in IL-4(+) T cells or IL-17(+) t T cells (P > 0.05) as compared to healthy donors. Moreover, the plasma levels of IFN-gamma in SLE patients were significantly higher than those in healthy controls ([68.9 +/- 29.1] pg/ml vs. [24.7 +/- 17.6] pg/ml, t = 5.430, P < 0.001). Moreover, in SLE patients, the percentage of autophagy in IFN-gamma T cells was positively correlated with the plasma levels of IFN-gamma (r = 0.344, P = 0.046), as well as the disease activity of patients with SLE (r = 0.379, P = 0.039). Conclusion: The results indicate that autophagy in IFN-gamma(+) T cells from SLE patients is activated, which might contribute to the persistence of T cells producing IFN-gamma, such as Thl cells, and consequently result in the high plasma levels of IFN-gamma, and then enhance the disease activity of SLE.