title: Angiogenic T cells are decreased in rheumatoid arthritis patients.
abstract: OBJECTIVE
  The mechanisms underlying the increased cardiovascular risk (CVR) of rheumatoid arthritis (RA) patients remain unclear. Since the recently discovered angiogenic T cells (Tang) could have a role in endothelial repair through cooperating with endothelial progenitor cells (EPC), the main aim of this study was to analyse the Tang and EPC populations in relation to disease-specific features and traditional CVR factors.
  
  
  METHODS
  Tang (CD3(+)CD31(+)CXCR4(+)) and EPC (CD34(+)VEGFR2(+)CD133(+)) populations were quantified by flow cytometry in peripheral blood samples from 103 RA patients and 18 matched healthy controls (HC). Clinical features and traditional CVR factors were obtained from clinical records, and 28-joint Disease Activity Score was used for measuring disease activity. Interferon (IFN) α serum levels were measured by immunoassays.
  
  
  RESULTS
  Tang and EPC were strongly decreased in RA patients. In HC, but not in patients, both populations were positively correlated and inversely related to low density lipoprotein- and total-cholesterol levels. Sex, diabetes, dyslipidaemia, hypertension or obesity did not significantly influence Tang in patients, although detected in smokers. However, Tang were closely related to disease activity, autoantibody positivity and IFNα levels. Multiple regression analysis adjusted for traditional CVR factors confirmed that only disease activity, age at diagnosis, antinuclear antibody positivity and smoking habit could predict Tang frequency. Finally, patients who had suffered a CV event since their RA diagnosis presented higher Tang decrease and IFNα levels than those who were CV event-free.
  
  
  CONCLUSIONS
  Disease-specific parameters, including disease activity, autoantibody profiles and IFNα levels, are associated with Tang decrease in RA, thus probably accounting for CVR.
authors.affiliation: Area of Immunology, Department of Functional Biology, University of Oviedo, Oviedo, Asturias, Spain.
authors.forename: Javier
authors.initials: J
authors.lastname: Rodríguez-Carrio
authors.affiliation: Department of Rheumatology, Hospital Universitario Central de Asturias, Oviedo, Asturias, Spain.
authors.forename: Mercedes
authors.initials: M
authors.lastname: Alperi-López
authors.affiliation: Area of Immunology, Department of Functional Biology, University of Oviedo, Oviedo, Asturias, Spain.
authors.forename: Patricia
authors.initials: P
authors.lastname: López
authors.affiliation: Department of Rheumatology, Hospital Universitario Central de Asturias, Oviedo, Asturias, Spain.
authors.forename: Sara
authors.initials: S
authors.lastname: Alonso-Castro
authors.affiliation: Department of Rheumatology, Hospital Universitario Central de Asturias, Oviedo, Asturias, Spain.
authors.forename: Francisco J
authors.initials: FJ
authors.lastname: Ballina-García
authors.affiliation: Area of Immunology, Department of Functional Biology, University of Oviedo, Oviedo, Asturias, Spain.
authors.forename: Ana
authors.initials: A
authors.lastname: Suárez
mesh_terms: D000328:Adult; D000368:Aged; D000974:Antibodies, Antinuclear / Q000276:immunology; D001172:Arthritis, Rheumatoid / Q000276:immunology* / Q000503:physiopathology; D001323:Autoantibodies / Q000276:immunology; D002318:Cardiovascular Diseases / Q000276:immunology*; D016022:Case-Control Studies; D066026:Endothelial Progenitor Cells / Q000276:immunology*; D005260:Female; D006801:Humans; D016898:Interferon-alpha / Q000276:immunology; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D018919:Neovascularization, Physiologic / Q000276:immunology*; D012044:Regression Analysis; D012307:Risk Factors; D012720:Severity of Illness Index; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D000974:Antibodies, Antinuclear; D001323:Autoantibodies; D016898:Interferon-alpha