Background Regulatory T cells (Treg cells)contribute to the process of immune suppression. Many studies reported that Treg cells were unbalanced in patients with systemic lupus erythematosus (SLE). The glucocorticoid-induced tumor necrosis factor receptor (GITR, also known as TNFRSF18) was constitutive expressed on Treg cells and involved in the regulation function of. Treg cells. GITR may play a role in the pathogenesis of SLE.Glucocorticoids Which used to treat SLE can inhibit a variety of immune cells and induce them apotosis. and. It may have affection on GITR expression or apotosis of Treg cells in SLE
Objectives To investigate the expression of glucocorticoid-induced tumor necrosis factor receptor (GITR) and apotosis of CD4+CD25+CD127-T cells in patients with systemic lupus erythematosus (SLE) and observe the affection by glucocorticoids
Methods 28 patients with a diagnosis of SLE according to the American College of Rheumatology (ACR) 1997 criteria were included in the study. The SLE patients were divided into active group (SLEDAI≥10) and inactive group (SLEDAI<10) according to the SLE disease activity index (SLEDAI).Active group included 15 patients; Inactive group included 13 patients. Clinical and laboratory data of patients with SLE were recorded. 12 normal volunteer without history of autoimmune diseases were also included. Peripheral blood CD4+CD25+CD127-T cells were isolatedby magnetic beads sorting.We classified them into two subgroups: the blank group and Therapeutic dose group (Dexamethasonedose 5×10-2 μg/ml and cultured for 48 hours).The expression of GITR and AnnexinV were analyzed by flow cytometry before and after cultured. The correlations between GITR levels,apotosis rates of these subsets and the clinic, laboratory parameters of SLE were analyzed.
Results GITR levels and apoptosis rates of Treg cells in patients with SLE were significantly higher than that in normal control group (t=2.209,P=0.033; t=2.037,P=0.049).The expression levels of GITR on Treg cells between blank groups and therapeutic dose groups were found no significant difference in patients with SLE (P>0.05),but in normal group the expression levels of GITR in therapeutic dose group were higher than that in blank group (P<0.05).After adding dexamethasone, The apoptosis rates of Treg cells were decreased in patients with SLE, the difference was statistically significant (P<0.05); But in normal control group, that was higher in therapeutic dose group than that in blank group (28.93±11.35 vs 40.06±15.25). The expression levels of GITR on Treg cells were significantly positively correlated with the disease active index in SLE (SLEDAI),but were correlated negatively with the C3.
Conclusions The GITR pathological expressed on Treg cells in SLE, it may be used asan immunologicalmarker of SLEdisease activity;glucocorticoidsmayregulateimmuneabnormalities by inhibitingTreg cellsapoptosis otherwise than GITR expression in SLE patients.
Disclosure of Interest None Declared
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