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Front Immunol ; 10: 1251, 2019.
Artículo en Inglés | MEDLINE | ID: mdl-31293564

RESUMEN

The administration of autologous tolerogenic dendritic cells (tolDC) has become a promising alternative for the treatment of autoimmune diseases, such as multiple sclerosis (MS). Specifically, the use of vitamin D3 for the generation of tolDC (vitD3-tolDC) constitutes one of the most widely studied approaches, as it has evidenced significant immune regulatory properties, both in vitro and in vivo. In this article, we generated human vitD3-tolDC from monocytes from healthy donors and MS patients, characterized in both cases by a semi-mature phenotype, secretion of IL-10 and inhibition of allogeneic lymphocyte proliferation. Additionally, we studied their transcriptomic profile and selected a number of differentially expressed genes compared to control mature and immature dendritic cells for their analysis. Among them, qPCR results validated CYP24A1, MAP7 and MUCL1 genes as biomarkers of vitD3-tolDC in both healthy donors and MS patients. Furthermore, we constructed a network of protein interactions based on the literature, which manifested that MAP7 and MUCL1 genes are both closely connected between them and involved in immune-related functions. In conclusion, this study evidences that MAP7 and MUCL1 constitute robust and potentially functional biomarkers of the generation of vitD3-tolDC, opening the window for their use as quality controls in clinical trials for MS.


Asunto(s)
Colecalciferol , Células Dendríticas , Tolerancia Inmunológica , Proteínas Asociadas a Microtúbulos , Mucinas , Esclerosis Múltiple , Humanos , Biomarcadores , Colecalciferol/metabolismo , Citocinas/metabolismo , Células Dendríticas/inmunología , Células Dendríticas/metabolismo , Susceptibilidad a Enfermedades , Inmunohistoquímica , Inmunofenotipificación , Mediadores de Inflamación/metabolismo , Proteínas Asociadas a Microtúbulos/metabolismo , Mucinas/metabolismo , Esclerosis Múltiple/etiología , Esclerosis Múltiple/metabolismo , Esclerosis Múltiple/patología , Transducción de Señal
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