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Mediators of Inflammation
Volume 2017, Article ID 2513829, 9 pages
Research Article

Patients with Systemic Lupus Erythematosus Show Increased Levels and Defective Function of CD69+ T Regulatory Cells

1Department of Immunology, Faculty of Medicine, UASLP, San Luis Potosí, SLP, Mexico
2Research Center for Health Sciences and Biomedicine, UASLP, San Luis Potosí, SLP, Mexico
3Laboratory of Genetics and Molecular Diagnostics, Faculty of Chemical Sciences, UASLP, San Luis Potosí, SLP, Mexico
4Regional Unit of Rheumatology and Osteoporosis, Hospital Central Dr. Ignacio Morones Prieto, San Luis Potosí, SLP, Mexico

Correspondence should be addressed to Roberto González-Amaro; xm.plsau@elaznogr

Received 30 March 2017; Revised 1 August 2017; Accepted 16 August 2017; Published 6 September 2017

Academic Editor: Alex Kleinjan

Copyright © 2017 Marlen Vitales-Noyola et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


T regulatory (Treg) cells have a key role in the pathogenesis of chronic inflammatory and autoimmune diseases. A CD4+CD69+ T cell subset has been described that behaves as Treg lymphocytes, exerting an important immune suppressive effect. In this study, we analyzed the levels and function of CD4+CD69+ Treg cells in patients with systemic lupus erythematosus (SLE). Blood samples were obtained from 22 patients with SLE and 25 healthy subjects. Levels of CD4+CD69+ Treg cells were analyzed by multiparametric flow cytometry, and their function was measured by an assay of suppression of lymphocyte activation and through the inhibition of cytokine synthesis. We found an increased percent of CD4+CD25varCD69+TGF-β+IL-10+Foxp3 lymphocytes in patients with SLE compared to controls. In addition, a significant diminution in the suppressive effect of these cells on the activation of autologous T lymphocytes was observed in most patients with SLE. Accordingly, CD69+ Treg cells from SLE patients showed a defective capability to inhibit the release of IL-2, IL-6, IL-10, and IL-17A by autologous lymphocytes. Our findings suggest that while CD4+CD69+ Treg lymphocyte levels are increased in SLE patients, these cells are apparently unable to contribute to the downmodulation of the autoimmune response and the tissue damage seen in this condition.