title: Immunologic effects in patients with psoriatic arthritis treated with cyclosporine A.
abstract: Twelve patients with psoriatic arthritis (PsA) and very active articular disease resistant to conventional second line therapy entered into a 6-month open study of cyclosporine A (CsA) at a starting dosage of 3 mg/kg/day. Comparisons of phenotypic characteristics of lymphocytes and response to mitogens of peripheral blood mononuclear cells (PBMC) were made between these patients with PsA before CsA therapy, 7 patients without prior 2nd line therapy, 14 untreated patients with psoriasis alone, and 61 healthy controls. We confirmed a significant reduction of the basal percentage of CD8+ cells and an increase in the CD4/CD8 ratio in patients with PsA before CsA therapy compared to controls. These abnormalities were not present in patients with PsA without prior 2nd line therapy and in patients with psoriasis alone. Peripheral blood activated T cells (CD3+, HLA-DR+), natural killer (NK) (CD3-, CD16+ and/or CD56+), total B and CD5+ B cells were decreased only in patients with PsA before CsA therapy. The reduction of non-MHC restricted cytotoxicity T (CD3+, CD16+ and/or CD56+) was observed in all the 3 groups of patients compared to controls. After the 6 months of CsA therapy we observed a significant increase of CD3+, HLA-DR+, CD3+, CD16+ and/or CD56+, total B, and CD20+, CD5+ cells in the 11 patients with PsA compared to pretreatment values. Contrary to azathioprine, CsA does not impair the NK cell population which has a protective role against cancer and viral infections.
authors.affiliation: 2nd Divisione di Medicina Interna (Unità Reumatologica), Reggio Emilia, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Boiardi
authors.forename: C
authors.initials: C
authors.lastname: Salvarani
authors.forename: P
authors.initials: P
authors.lastname: Macchioni
authors.forename: M
authors.initials: M
authors.lastname: Casadei Maldini
authors.forename: R
authors.initials: R
authors.lastname: Mancini
authors.forename: E
authors.initials: E
authors.lastname: Beltrandi
authors.forename: F
authors.initials: F
authors.lastname: Rossi
authors.forename: L
authors.initials: L
authors.lastname: Lodi
authors.forename: I
authors.initials: I
authors.lastname: Portioli
mesh_terms: D015703:Antigens, CD / Q000032:analysis; D018951:Antigens, CD20; D000944:Antigens, Differentiation, B-Lymphocyte / Q000032:analysis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis; D015535:Arthritis, Psoriatic / Q000188:drug therapy* / Q000453:epidemiology / Q000276:immunology*; D017252:CD3 Complex / Q000032:analysis; D016516:CD4-CD8 Ratio; D019002:CD56 Antigen; D016572:Cyclosporine / Q000627:therapeutic use*; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology / Q000473:pathology; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000473:pathology; D008213:Lymphocyte Activation; D010641:Phenotype; D011446:Prospective Studies; D017452:Receptors, IgG / Q000032:analysis; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology
chemical_list: D015703:Antigens, CD; D018951:Antigens, CD20; D000944:Antigens, Differentiation, B-Lymphocyte; D000945:Antigens, Differentiation, T-Lymphocyte; D017252:CD3 Complex; D019002:CD56 Antigen; D006684:HLA-DR Antigens; D017452:Receptors, IgG; D016572:Cyclosporine