Induction of Th17 lymphocytes and treg cells by monocyte-derived dendritic cells in patients with rheumatoid arthritis and systemic lupus erythematosus
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Dendritic cells (DCs) have a key role in the regulation of immune response. We herein explored, in patients with inflammatory diseases, the role of monocyte derived DC%27s (mo-DCs) on the generation of Th17 and T regulatory (Treg) lymphocytes. Peripheral blood was obtained from thirty-five patients with rheumatoid arthritis (RA), twelve with systemic lupus erythematosus (SLE), and twenty healthy subjects. Mo-DCs were generated under standard (IL-4/GM-CSF) or tolerogenic (IL-4/GM-CSF plus recombinant P-selectin or PD-1 or IL-10) conditions, and their ability to induce Th17 and Treg lymphocytes was tested. We detected that mo-DCs from patients with RA showed an enhanced release of IL-6 and IL-23 as well as an increased capability to induce Th17 cells. Although mo-DCs from SLE patients also released high levels of IL-6/IL-23, it did not show an increased ability to induce Th17 lymphocytes. In addition, mo-DCs, from patients with RA and SLE generated under the engagement of PSGL-1, showed a defective capability to induce Foxp3 Treg cells. A similar phenomenon was observed in SLE, when DC%27s cells were generated under PDL-1 engagement. Our data indicate that DCs from patients with rheumatic inflammatory disease show an aberrant function that may have an important role in the pathogenesis of these conditions. © 2013 Lizbeth Estrada-Capetillo et al.
Dendritic cells (DCs) have a key role in the regulation of immune response. We herein explored, in patients with inflammatory diseases, the role of monocyte derived DC%27s (mo-DCs) on the generation of Th17 and T regulatory (Treg) lymphocytes. Peripheral blood was obtained from thirty-five patients with rheumatoid arthritis (RA), twelve with systemic lupus erythematosus (SLE), and twenty healthy subjects. Mo-DCs were generated under standard (IL-4/GM-CSF) or tolerogenic (IL-4/GM-CSF plus recombinant P-selectin or PD-1 or IL-10) conditions, and their ability to induce Th17 and Treg lymphocytes was tested. We detected that mo-DCs from patients with RA showed an enhanced release of IL-6 and IL-23 as well as an increased capability to induce Th17 cells. Although mo-DCs from SLE patients also released high levels of IL-6/IL-23, it did not show an increased ability to induce Th17 lymphocytes. In addition, mo-DCs, from patients with RA and SLE generated under the engagement of PSGL-1, showed a defective capability to induce Foxp3%2b Treg cells. A similar phenomenon was observed in SLE, when DC%27s cells were generated under PDL-1 engagement. Our data indicate that DCs from patients with rheumatic inflammatory disease show an aberrant function that may have an important role in the pathogenesis of these conditions. © 2013 Lizbeth Estrada-Capetillo et al.
Dendritic cells (DCs) have a key role in the regulation of immune response. We herein explored, in patients with inflammatory diseases, the role of monocyte derived DC's (mo-DCs) on the generation of Th17 and T regulatory (Treg) lymphocytes. Peripheral blood was obtained from thirty-five patients with rheumatoid arthritis (RA), twelve with systemic lupus erythematosus (SLE), and twenty healthy subjects. Mo-DCs were generated under standard (IL-4/GM-CSF) or tolerogenic (IL-4/GM-CSF plus recombinant P-selectin or PD-1 or IL-10) conditions, and their ability to induce Th17 and Treg lymphocytes was tested. We detected that mo-DCs from patients with RA showed an enhanced release of IL-6 and IL-23 as well as an increased capability to induce Th17 cells. Although mo-DCs from SLE patients also released high levels of IL-6/IL-23, it did not show an increased ability to induce Th17 lymphocytes. In addition, mo-DCs, from patients with RA and SLE generated under the engagement of PSGL-1, showed a defective capability to induce Foxp3%2b Treg cells. A similar phenomenon was observed in SLE, when DC's cells were generated under PDL-1 engagement. Our data indicate that DCs from patients with rheumatic inflammatory disease show an aberrant function that may have an important role in the pathogenesis of these conditions. © 2013 Lizbeth Estrada-Capetillo et al.
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gamma interferon; interleukin 10; interleukin 21; interleukin 23; interleukin 4; interleukin 6; P selectin glycoprotein ligand 1; PADGEM protein; transcription factor FOXP3; cytokine; adult; article; blood sampling; CD4 T lymphocyte; clinical article; controlled study; cytokine release; dendritic cell; disease activity; female; human; male; monocyte; monocyte derived dendritic cell; pathogenesis; priority journal; regulatory T lymphocyte; rheumatoid arthritis; systemic lupus erythematosus; Th17 cell; adolescent; cell differentiation; coculture; cytology; immunology; immunophenotyping; metabolism; middle aged; phenotype; rheumatoid arthritis; systemic lupus erythematosus; young adult; Adolescent; Adult; Arthritis, Rheumatoid; Cell Differentiation; Coculture Techniques; Cytokines; Dendritic Cells; Female; Humans; Immunophenotyping; Lupus Erythematosus, Systemic; Middle Aged; Phenotype; T-Lymphocytes, Regulatory; Th17 Cells; Young Adult
gamma interferon; interleukin 10; interleukin 21; interleukin 23; interleukin 4; interleukin 6; P selectin glycoprotein ligand 1; PADGEM protein; transcription factor FOXP3; cytokine; adult; article; blood sampling; CD4+ T lymphocyte; clinical article; controlled study; cytokine release; dendritic cell; disease activity; female; human; male; monocyte; monocyte derived dendritic cell; pathogenesis; priority journal; regulatory T lymphocyte; rheumatoid arthritis; systemic lupus erythematosus; Th17 cell; adolescent; cell differentiation; coculture; cytology; immunology; immunophenotyping; metabolism; middle aged; phenotype; rheumatoid arthritis; systemic lupus erythematosus; young adult; Adolescent; Adult; Arthritis, Rheumatoid; Cell Differentiation; Coculture Techniques; Cytokines; Dendritic Cells; Female; Humans; Immunophenotyping; Lupus Erythematosus, Systemic; Middle Aged; Phenotype; T-Lymphocytes, Regulatory; Th17 Cells; Young Adult
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