Analysis of CXCR5 + Th17 cells in relation to disease activity and TNF inhibitor therapy in Rheumatoid Arthritis.

Autor: Singh D; Division of Rheumatology, Department of Medicine, University of Pittsburgh, 3500 Terrace St, Pittsburgh, PA 15261, USA., Henkel M; Division of Rheumatology, Department of Medicine, University of Pittsburgh, 3500 Terrace St, Pittsburgh, PA 15261, USA., Sendon B; Division of Rheumatology, Department of Medicine, University of Pittsburgh, 3500 Terrace St, Pittsburgh, PA 15261, USA., Feng J; Epidemiology Data Coordinating Center, Graduate School of Public Health, University of Pittsburgh, 130 DeSoto St, Pittsburgh, PA 15261, USA., Fabio A; Epidemiology Data Coordinating Center, Graduate School of Public Health, University of Pittsburgh, 130 DeSoto St, Pittsburgh, PA 15261, USA., Metes D; Department of Surgery, Starzl Transplantation Institute, University of Pittsburgh, PA, USA., Moreland LW; Division of Rheumatology, Department of Medicine, University of Pittsburgh, 3500 Terrace St, Pittsburgh, PA 15261, USA., McGeachy MJ; Division of Rheumatology, Department of Medicine, University of Pittsburgh, 3500 Terrace St, Pittsburgh, PA 15261, USA.
Jazyk: angličtina
Zdroj: Scientific reports [Sci Rep] 2016 Dec 22; Vol. 6, pp. 39474. Date of Electronic Publication: 2016 Dec 22.
DOI: 10.1038/srep39474
Abstrakt: Th17 and TfH cells are thought to promote tissue inflammation and autoantibody production, respectively, in autoimmune diseases including rheumatoid arthritis (RA). TfH cells that co-express Th17 markers (CXCR5 + Th17) encompass both of these pathogenic functions, and are increased in some human autoimmune settings including juvenile dermatomyositis. We investigated CXCR5 + Th17 cells in RA subjects with stable or active disease and before and after TNF inhibitor therapy. CXCR5 + Th17 cell frequency was increased in RA compared to healthy controls, but other helper T cell subsets were not different. CXCR5 + Th17 cells correlated with disease activity in subjects with active RA prior to initiation of TNF inhibitor therapy. Baseline CXCR5 + Th17 cells also correlated with numbers of swollen joints as late as one year post-therapy. CXCR5 + Th17 cell frequencies were unaltered by TNF blockade and in fact remained remarkably stable within individuals. We conclude that CXCR5 + Th17 cells are not a direct target of TNF blockade and therefore cannot serve as a biomarker of current disease activity. However, basal CXCR5 + Th17 cell frequency may indicate underlying differences in disease phenotype between patients and predict ultimate success of TNF inhibitor therapy.
Databáze: MEDLINE
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