Immunoregulation therapy changes the frequency of interleukin (IL)‐22+CD4+ T cells in systemic lupus erythematosus patients

T cell and T cell‐related cytokine abnormalities are involved in the pathogenesis of systemic lupus erythematosus (SLE). Our previous study showed that the interleukin (IL)‐22⁺CD4⁺T cells and IL‐22 play an important role in the pathogenesis of SLE. In this study, we aimed to investigate the effects of glucocorticoids (GCs) and immunodepressant agents on IL‐22 and IL‐22‐producing T cell subsets in SLE patients. The frequencies of peripheral blood T helper type 22 (Th22), IL‐22⁺Th17, IL‐22⁺Th1 and Th17 cells and the concentrations of serum IL‐22, IL‐17 and interferon (IFN)‐γ in SLE patients receiving 4 weeks of treatment with cyclophosphamide (CYC), methylprednisolone and hydroxychloroquine (HCQ) were characterized by flow cytometry analysis and enzyme‐linked immunosorbent assay (ELISA). The frequencies of Th22, IL‐22⁺ Th17 and Th17 cells and the concentrations of IL‐22 and IL‐17 were reduced in response to the drugs methylprednisolone, cyclophosphamide and hydroxychloroquine for 4 weeks in the majority of SLE patients. However, the percentage of Th1 cells showed no change. No differences in the levels of IL‐22 and IL‐22⁺CD4⁺ T cells were found between non‐responders and health controls either before or after therapy. IL‐22 levels were correlated positively with Th22 cells in SLE patients after treatment. These results suggest that elevated IL‐22 is correlated with IL‐22⁺CD4⁺T cells, especially Th22 cells, and may have a co‐operative or synergetic function in the immunopathogenesis of SLE. GC, CYC and HCQ treatment may regulate the production of IL‐22, possibly by correcting the IL‐22⁺CD4⁺T cells polarizations in SLE, thus providing new insights into the mechanism of GC, CYC and HCQ in the treatment of SLE.