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      Altered Th17 cells and Th17/regulatory T-cell ratios indicate the subsequent conversion from undifferentiated connective tissue disease to definitive systemic autoimmune disorders.

      1 , , , , , , , ,
      Human immunology
      (Scleroderma-70 antigen, DNA Topoisomerase I), ANA, ANCA, APC, C-reactive protein, CCP, CNS, CRP, ELISA, ENA, FITC, IL-10 producing Type-1 regulatory T-cells, MCTD, NKT, PBMC, PE, PM/DM, RA, RF, SAID, SLE, SS, SSc, Scl-70, Sjögren’s syndrome, Sm, Smith antigen, T-helper cell, Tc-DTPA, Th, Tr1, Treg, U1 ribonucleoprotein, U1RNP, UCTD, aCL, allophycocyanin, anti-cardiolipin, anti-neutrophil cytoplasmic antibodies, anti-nuclear antibody, central nervous system, cyclic citrullinated peptide, double-stranded deoxyribonucleic acid, dsDNA, enzyme-linked immunosorbent assay, extractable nuclear antigen, fluorescein isothiocyanate, mixed connective tissue disease, nTreg, natural killer T cell, natural regulatory T cell, peripheral blood mononuclear cell, phycoerythrin, polymyositis/dermatomyositis, regulatory T cell, rheumatoid arthritis, rheumatoid factor, systemic autoimmune disease, systemic lupus erythematosus, systemic sclerosis, technetium-diethylene-triamine-pentaacetate, undifferentiated connective tissue disease

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          Abstract

          A shift in the balance between Th17-cells and regulatory T-cells (Treg) is an important feature of systemic autoimmune diseases (SAID), and may also contribute to their development. Hereby, we assessed the distribution of peripheral Th17 and Treg-cells in patients with undifferentiated connective tissue disease (UCTD), the forerunner of SAIDs and followed these parameters during the development towards definitive SAIDs. Fifty-one UCTD patients were investigated and followed-up for 3 years. Flow cytometry was used to identify and follow three cell-populations: Th17-cells (CD4+IL-17+ T-cells), natural regulatory T-cells (CD4(+)CD25(bright)FoxP3(+); nTregs) and IL-10 producing Type-1 regulatory T-cells (CD4+IL-10+ T-cells; Tr1). Altogether 37.3% of these patients progressed into SAIDs. Th17-cells were increased in UCTD vs. controls, which further increased in those, whom developed SAIDs eventually. The Th17/nTreg ratio gradually increased from controls through UCTD patients, reaching the highest values in SAID-progressed patients. Regarding the Th17/Tr1 ratios, a similar tendency was observed moreover Th17/Tr1 could distinguish between UCTD patients with, or without subsequent SAID progression in a very early UCTD stage. Various immunoserological markers showed association with Th17 and Th17/nTreg at baseline, indicating the consecutive development of a distinct SAID. The derailed Th17/Treg balance may contribute to disease progression therefore could function as a prognostic marker.

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          Author and article information

          Journal
          Hum. Immunol.
          Human immunology
          1879-1166
          0198-8859
          Dec 2013
          : 74
          : 12
          Affiliations
          [1 ] Institute of Immunology, Rikshospitalet, Oslo University Hospital, Oslo, Norway. Electronic address: szodoray@gmail.com.
          Article
          S0198-8859(13)00228-0
          10.1016/j.humimm.2013.08.003
          23974054
          6a58b193-af8d-4bb4-bf81-085c4c2d7157
          Copyright © 2013 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.
          History

          (Scleroderma-70 antigen, DNA Topoisomerase I),ANA,ANCA,APC,C-reactive protein,CCP,CNS,CRP,ELISA,ENA,FITC,IL-10 producing Type-1 regulatory T-cells,MCTD,NKT,PBMC,PE,PM/DM,RA,RF,SAID,SLE,SS,SSc,Scl-70,Sjögren’s syndrome,Sm,Smith antigen,T-helper cell,Tc-DTPA,Th,Tr1,Treg,U1 ribonucleoprotein,U1RNP,UCTD,aCL,allophycocyanin,anti-cardiolipin,anti-neutrophil cytoplasmic antibodies,anti-nuclear antibody,central nervous system,cyclic citrullinated peptide,double-stranded deoxyribonucleic acid,dsDNA,enzyme-linked immunosorbent assay,extractable nuclear antigen,fluorescein isothiocyanate,mixed connective tissue disease,nTreg,natural killer T cell,natural regulatory T cell,peripheral blood mononuclear cell,phycoerythrin,polymyositis/dermatomyositis,regulatory T cell,rheumatoid arthritis,rheumatoid factor,systemic autoimmune disease,systemic lupus erythematosus,systemic sclerosis,technetium-diethylene-triamine-pentaacetate,undifferentiated connective tissue disease

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