title: Immunoregulation therapy changes the frequency of interleukin (IL)-22+ CD4+ T cells in systemic lupus erythematosus patients.
abstract: 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.
authors.affiliation: Department of Rheumatology, The First Hospital, Jilin University, Changchun, China.
authors.forename: L
authors.initials: L
authors.lastname: Zhao
authors.forename: H
authors.initials: H
authors.lastname: Ma
authors.forename: Z
authors.initials: Z
authors.lastname: Jiang
authors.forename: Y
authors.initials: Y
authors.lastname: Jiang
authors.forename: N
authors.initials: N
authors.lastname: Ma
mesh_terms: D000293:Adolescent; D000328:Adult; D015704:CD4 Antigens / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D002454:Cell Differentiation / Q000187:drug effects; D019070:Cell Lineage / Q000187:drug effects; D003520:Cyclophosphamide / Q000008:administration & dosage; D005260:Female; D006706:Homeostasis; D006801:Humans; D006886:Hydroxychloroquine / Q000008:administration & dosage; D056747:Immunomodulation; D007166:Immunosuppressive Agents / Q000008:administration & dosage; D007167:Immunotherapy / Q000379:methods*; D007371:Interferon-gamma / Q000097:blood; D007378:Interleukins / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000276:immunology* / Q000628:therapy*; D008297:Male; D008775:Methylprednisolone / Q000008:administration & dosage; D018417:Th1 Cells / Q000187:drug effects* / Q000276:immunology; D055815:Young Adult; D000097043:Interleukin-22
chemical_list: D015704:CD4 Antigens; D003520:Cyclophosphamide; D006886:Hydroxychloroquine; D007166:Immunosuppressive Agents; D007371:Interferon-gamma; D007378:Interleukins; D008775:Methylprednisolone; D000097043:Interleukin-22
keywords: IL-22; Th22; cyclophosphamide; systemic lupus erythematosus