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Type: Artigo
Title: Tolerogenic Vaccination With Mog/vitd Overcomes Aggravating Effect Of C-albicans In Experimental Encephalomyelitis
Author: Fraga-Silva
Thais F. C.; Mimura
Luiza A. N.; Zorzella-Pezavento
Sofia F. G.; Ishikawa
Larissa L. W.; Franca
Thais G. D.; Thome
Rodolfo; Verinaud
Liana; Arruda
Maria S. P.; Sartori
Abstract: Multiple sclerosis (MS) is an immune-mediated demyelinating disorder of the central nervous system (CNS). We described that Candida albicans (Ca) aggravates experimental autoimmune encephalomyelitis (EAE) that is a model to study MS. We also observed that vaccination with a myelin peptide (MOG) in the presence of vitamin D (VitD) protected mice against EAE. In this work, we investigated whether Ca infection interferes with the efficacy of this vaccine. MethodsEAE was induced in C57BL/6 female mice previously vaccinated with MOG+VitD and then infected 3 days before encephalomyelitis induction. ResultsVaccination was able to control EAE development in infected mice. These animals gained weight, and only a few progressed to very low clinical scores. Protection was confirmed by a lower inflammatory infiltration in the CNS and was also associated with a reduced production of encephalitogenic cytokines by spleen and CNS cell cultures. The elevated percentage of CD25(+)FoxP3(+) cells suggests that regulatory T cells are involved in the protection. Adoptive transfer of splenocytes from mice vaccinated with MOG+VitD supports the view that protection is mediated by immunoregulatory cells. ConclusionTogether, these experiments provide evidence demonstrating that EAE can be prevented by the inverse vaccination with MOG+VitD even in the presence of a disease-aggravating infectious agent.
Subject: Active Vitamin D
Disseminated Candidiasis
Multiple Sclerosis
Myelin Oligodendrocyte Glycoprotein
Tolerogenic Vaccination
Editor: Wiley-Blackwell
Citation: Cns Neuroscience & Therapeutics. Wiley-blackwell, v. 22, p. 807 - 816, 2016.
Rights: fechado
Identifier DOI: 10.1111/cns.12572
Date Issue: 2016
Appears in Collections:Unicamp - Artigos e Outros Documentos

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