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Marlen Vitales-Noyola [1; 2] and Brenda Oceguera-Maldonado [1; 2] and Perla Niño-Moreno [2; 3] and Nubia Baltazar-Benítez [1; 2] and Lourdes Baranda [1; 2] and Esther Layseca-Espinosa [1; 2] and Carlos Abud-Mendoza [4] and Roberto González-Amaro [1; 2]

Academic Editor: Alex Kleinjan

1, Department of Immunology, Faculty of Medicine, UASLP, San Luis Potosí, SLP, Mexico, uaslp.mx

2, Research Center for Health Sciences and Biomedicine, UASLP, San Luis Potosí, SLP, Mexico, uaslp.mx

3, Laboratory of Genetics and Molecular Diagnostics, Faculty of Chemical Sciences, UASLP, San Luis Potosí, SLP, Mexico, uaslp.mx

4, Regional Unit of Rheumatology and Osteoporosis, Hospital Central Dr. Ignacio Morones Prieto, San Luis Potosí, SLP, Mexico, hospitalcentral.gob.mx

Received Mar 30, 2017; Revised Aug 1, 2017; Accepted Aug 16, 2017

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.

1. Introduction

Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder characterized by loss of tolerance to self-antigens and synthesis of many different auto-antibodies with the involvement of multiple organ systems, including the skin, kidney, blood vessels, and central nervous system [1, 2]. The pathogenesis of this condition is complex, and the loss of tolerance to self-antigens observed in these patients is a consequence of multiple genetic risk factors, environmental influences, and defects in immune regulatory mechanisms, among others [1, 2].

Different mechanisms that are able to downregulate the immune response have been described, including the T regulatory (Treg) cells [3]. These cells are able to suppress the activation and proliferation of effector lymphocytes, exerting thus a key role in the pathogenesis of autoimmune and chronic inflammatory conditions [3]. Several subtypes of Treg lymphocytes have been described. Natural T regulatory (nTreg) cells show a characteristic phenotype (CD4+CD25highFoxp3+) and exert their suppressive effect on effector T cells through different mechanisms, including the synthesis of immune modulatory cytokines (TGF-β, IL-10, and IL-35) [3–7]. These Foxp3+ regulatory cells can be originated directly from the thymus (tTreg cells) or in the periphery (pTreg cells), by the differentiation of conventional naïve CD4+ cells. In addition, Treg cells with this phenotype can be generated in vitro (induced or iTreg cells)...

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