BACKGROUND AND OBJECTIVE: It is fairly well established that T-helper (TH)((1)) cells play a role in the pathogenesis of organ-specific autoimmune diseases, while their role and their relationship with TH((2)) cells is far from being defined in systemic lupus erythematosus (SLE). To address this issue, six female patients who fulfilled the American Rheumatism Association criteria for the diagnosis of SLE were studied. DESIGN AND METHODS: We analyzed the intracellular production of cytokines by T-cells from the peripheral blood (PB). Then, we established T-cell clones (TCC) from the peripheral blood (PB) of all cases as well as from the synovial fluid of one patient with an articular flare-up. RESULTS: The percentages of IL-4 positive and IFN-g positive PB T-cells were not different between SLE patients and normal controls. When 93 TCC (67 CD4(+), 23 CD8(+)) from the PB of 5 different SLE patients were compared to 118 TCC (94 CD4(+), 23 CD8(+)) from 5 healthy controls no statistical difference was observed between SLE and controls in terms of TH((1)), TH((2)) or TH((0)) phenotype. However, SLE clones showed a reduced ability to secrete IL-10 (p = 0. 002). In contrast, the analysis of the 30 clones obtained from synovial fluid revealed that 11/23 CD4(+) clones were TH((1)), 12/23 were TH((0)), 2/7 CD8(+ )clones were TH((1)) and 5/7 were TH((0)). No TH((2)) clones were obtained from the synovial fluid. INTERPRETATION AND CONCLUSIONS: The data suggest that the T-cell subsets operating in actively inflamed organs of SLE may belong to the TH((1)) and TH((0)) subsets.
BACKGROUND AND OBJECTIVE: It is fairly well established that T-helper (TH)((1)) cells play a role in the pathogenesis of organ-specific autoimmune diseases, while their role and their relationship with TH((2)) cells is far from being defined in systemic lupus erythematosus (SLE). To address this issue, six female patients who fulfilled the American Rheumatism Association criteria for the diagnosis of SLE were studied. DESIGN AND METHODS: We analyzed the intracellular production of cytokines by T-cells from the peripheral blood (PB). Then, we established T-cell clones (TCC) from the peripheral blood (PB) of all cases as well as from the synovial fluid of one patient with an articular flare-up. RESULTS: The percentages of IL-4 positive and IFN-g positive PB T-cells were not different between SLEpatients and normal controls. When 93 TCC (67 CD4(+), 23 CD8(+)) from the PB of 5 different SLEpatients were compared to 118 TCC (94 CD4(+), 23 CD8(+)) from 5 healthy controls no statistical difference was observed between SLE and controls in terms of TH((1)), TH((2)) or TH((0)) phenotype. However, SLE clones showed a reduced ability to secrete IL-10 (p = 0. 002). In contrast, the analysis of the 30 clones obtained from synovial fluid revealed that 11/23 CD4(+) clones were TH((1)), 12/23 were TH((0)), 2/7 CD8(+ )clones were TH((1)) and 5/7 were TH((0)). No TH((2)) clones were obtained from the synovial fluid. INTERPRETATION AND CONCLUSIONS: The data suggest that the T-cell subsets operating in actively inflamed organs of SLE may belong to the TH((1)) and TH((0)) subsets.
Authors: E Robak; H Niewiadomska; T Robak; J Bartkowiak; J Z Błoński; A Woźniacka; L Pomorski; A Sysa-Jedrezejowska Journal: Mediators Inflamm Date: 2001-08 Impact factor: 4.711