Regulatory T cell induction during Plasmodium chabaudi infection modifies the clinical course of experimental autoimmune encephalomyelitis
| Autor: | Ana Leda F. Longhini, Fabio T. M. Costa, Stefanie C. P. Lopes, Leonilda M.B. Santos, Yara C. Blanco, Fernando Pradella, Rafael L. Talaisys, Alessandro S. Farias |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2011 |
| Předmět: |
Adoptive cell transfer
Encephalomyelitis Autoimmune Experimental Regulatory T cell Cell Survival Immunology lcsh:Medicine Autoimmunity Biology Protozoology medicine.disease_cause Microbiology T-Lymphocytes Regulatory Plasmodium chabaudi Mice medicine Animals Humans IL-2 receptor lcsh:Science Autoimmune disease Multidisciplinary Multiple sclerosis Experimental autoimmune encephalomyelitis lcsh:R Interleukin-2 Receptor alpha Subunit medicine.disease biology.organism_classification Malaria Mice Inbred C57BL medicine.anatomical_structure Gene Expression Regulation Disease Progression Cytokines Parasitology lcsh:Q Research Article |
| Zdroj: | PLoS ONE, Vol 6, Iss 3, p e17849 (2011) PLoS ONE |
| ISSN: | 1932-6203 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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