Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/107723
Type: Artigo de periódico
Title: Regulatory T Cell Induction During Plasmodium Chabaudi Infection Modifies The Clinical Course Of Experimental Autoimmune Encephalomyelitis
Author: Farias A.S.
Talaisys R.L.
Blanco Y.C.
Lopes S.C.P.
Longhini A.L.F.
Pradella F.
Santos L.M.B.
Costa F.T.M.
Abstract: Background: Experimental autoimmune encephalomyelitis (EAE) is used as an animal model for human multiple sclerosis (MS), which is an inflammatory demyelinating autoimmune disease of the central nervous system characterized by activation of Th1 and/or Th17 cells. Human autoimmune diseases can be either exacerbated or suppressed by infectious agents. Recent studies have shown that regulatory T cells play a crucial role in the escape mechanism of Plasmodium spp. both in humans and in experimental models. These cells suppress the Th1 response against the parasite and prevent its elimination. Regulatory T cells have been largely associated with protection or amelioration in several autoimmune diseases, mainly by their capacity to suppress proinflammatory response. Methodology/Principal Findings: In this study, we verified that CD4+CD25+ regulatory T cells (T regs) generated during malaria infection (6 days after EAE induction) interfere with the evolution of EAE. We observed a positive correlation between the reduction of EAE clinical symptoms and an increase of parasitemia levels. Suppression of the disease was also accompanied by a decrease in the expression of IL-17 and IFN-γ and increases in the expression of IL-10 and TGF-β1 relative to EAE control mice. The adoptive transfer of CD4+CD25+ cells from P. chabaudi-infected mice reduced the clinical evolution of EAE, confirming the role of these T regs. Conclusions/Significance: These data corroborate previous findings showing that infections interfere with the prevalence and evolution of autoimmune diseases by inducing regulatory T cells, which regulate EAE in an apparently non-specific manner. © 2011 Farias et al.
Editor: 
Rights: aberto
Identifier DOI: 10.1371/journal.pone.0017849
Address: http://www.scopus.com/inward/record.url?eid=2-s2.0-79953056711&partnerID=40&md5=c452b6be1e050d2ee4c83f8f8c1d2f6e
Date Issue: 2011
Appears in Collections:Unicamp - Artigos e Outros Documentos

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.