ArticlePloS one2011
Regulatory T cell induction during Plasmodium chabaudi infection modifies the clinical course of experimental autoimmune encephalomyelitis.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 39 citations in OpenAlex.
- Anti-NMDAR encephalitis following malaria: expanding the spectrum of post-malarial neurological syndromes.Frontiers in immunology · 2026Article
- Microbial (co)infections: Powerful immune influencers.PLoS pathogens · 2022Review
- Article
- Interleukin-5 Mediates Parasite-Induced Protection against Experimental Autoimmune Encephalomyelitis: Association with Induction of Antigen-Specific CD4Frontiers in immunology · 2017Article
- Parasite-Derived Proteins for the Treatment of Allergies and Autoimmune Diseases.Frontiers in microbiology · 2017Review
- Immune Modulation and Prevention of Autoimmune Disease by Repeated Sequences from Parasites Linked to Self Antigens.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016Article
- Experimental autoimmune encephalomyelitis development is aggravated by Candida albicans infection.Journal of immunology research · 2015Article
- Infusion of Sulfosuccinimidyl-4-[N-maleimidomethyl]cyclohexane-1-carboxylate-Conjugated MOG35-55-Coupled Spleen Cells Effectively Prevents and Reverses Experimental Autoimmune Encephalomyelitis in Mice.Journal of immunology research · 2015Article
- Article
- In vivo administration of TLR9 agonist reduces the severity of experimental autoimmune encephalomyelitis. The role of plasmacytoid dendritic cells and B lymphocytes.CNS neuroscience & therapeutics · 2014Article
- Exacerbation of autoimmune neuro-inflammation in mice cured from blood-stage Plasmodium berghei infection.PloS one · 2014Article
- Vitamin D3 induces IDO+ tolerogenic DCs and enhances Treg, reducing the severity of EAE.CNS neuroscience & therapeutics · 2013Article
- Chloroquine treatment enhances regulatory T cells and reduces the severity of experimental autoimmune encephalomyelitis.PloS one · 2013Article
- Infection and autoimmunity: Lessons of animal models.European journal of microbiology & immunology · 2011Review
- Phenotype and function of regulatory T cells in the genital tract.Current trends in immunology · 2011Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExperimental 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
findingsIn 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.
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