Helper T cell 17-regulatory T cell equilibrium in patients with systemic lupus erythematosus

Objective To investigate the changes and clinical significance of the equilibrium of peripheral blood helper T cell 17 (Th17)-regulatory T cell (Treg) in patients with systemic lupus erythematosus (SLE).Methods Forty patients with active SLE,40 clinically stable SLE patienls and 20 healthy volunteers were enrolled in this study.Changes in peripheral blood Th17/Treg cell ratio and its correlation with disease activity were determined following detection of Th17 cells and Treg cells by flow cytometry.Real-time fluorescent quantitative PCR was employed to examine the expression of retinoic acid related solitary nucleus receptor (RORγt) and fork wing spiral transcription factor (Foxp3) mRNAs,the genes that govern regulation of Th17 and Treg cells,in peripheral mononuclear cell (PBMC).Results Patients with active SLE had higher percentage of Th17 cells in peripheral blood compared with those without active SLE [(1.86±0.96) ％ vs (1.05±0.40)％,P＜0.01] and healthy controls [(0.80±0.33)％,P<0.01],and lower percentage of CD4-CD25+Foxp3+Treg cells compared with those without active SLE [(1.95±0.85) ％ vs (4.22± 1.34)％,P＜0.01] and healthy controls [(6.04+1.49)％,P＜0.01].The ratio of Th17/Treg cells increased during the active state when compared with clinically stable period [(0.97±0.55) vs (0.25±0.38),P＜0.01] and healthy controls [(0.13±0.07),P＜0.O1],which was positively correlated with SLE disease activity index score (r=0.69,P＜0.01).Furthermore,SLE patients presented higher RORγt mRNA expression [(7.61±5.39) vs (3.51±3.52),P＜0.05] and lower Foxp3 mRNA expression ([4.67±4.23] vs [11.67±5.09],P＜0.05) as compared with healthy controls.Conclusion Patients with active SLE have more Th17 cells and up-regulating RORγt mRNA expression,but less Treg cells and down-regulating Foxp3 mRNA expression leading to imbalance of Th17/Treg cell ratio in peripheral blood.Increased differentiated Th17 cell count and reduced Foxp3 mRNA may be involved in the pathogenesis of SLE. Key words: Lupus erythematosus, systemic; T-lymphocytes, helper-induced; T-lymphocytes,regulatory