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Myelin Oligodendrocyte Glycoprotein MOG35-55 Induced Experimental Autoimmune Encephalomyelitis EAE in C57BL/6 Mice
Published on: April 15, 2014
Murine Cytomegalovirus Infection Induces Susceptibility to EAE in Resistant BALB/c Mice
Jelena Milovanovic1, Branka Popovic2, Marija Milovanovic3
1Center for Molecular Medicine and Stem Cell Research, Faculty of Medical Sciences, University of Kragujevac, Kragujevac, Serbia; Faculty of Medical Sciences, Institute of Histology, University of Kragujevac, Kragujevac, Serbia.
Abstract:
In contrast to C57BL/6 mice, BALB/c mice are relatively resistant to the induction of experimental autoimmune encephalomyelitis (EAE) after challenge with MOG35-55 peptide. Here, we provide the first evidence that infection with murine cytomegalovirus (MCMV) in adulthood abrogates this resistance. Infected BALB/c mice developed clinical and histological signs similar to those seen in susceptible C57BL/6 mice. In addition to CD4+ cells, large proportion of cells in the infiltrate of diseased BALB/c mice was CD8+, similar with findings in multiple sclerosis. CD8+ cells that responded to ex vivo restimulation with MOG35-55 were not specific for viral epitopes pp89 and m164. MCMV infection favors proinflammatory type of dendritic cells (CD86+CD40+CD11c+) in the peripheral lymph organs, M1 type of microglia in central nervous system, and increases development of Th1/Th17 encephalitogenic cells. This study indicates that MCMV may enhance autoimmune neuropathology and abrogate inherent resistance to EAE in mouse strain by enhancing proinflammatory phenotype of antigen-presenting cells, Th1/Th17, and CD8 response to MOG35-55.
Insights
Murine cytomegalovirus (MCMV) infection breaks resistance to experimental autoimmune encephalomyelitis (EAE) in BALB/c mice. MCMV infection promotes inflammation and CD8+ T cell responses, mimicking multiple sclerosis pathology.
Area of Science:
- Neuroimmunology
- Virology
- Immunology
Background:
- BALB/c mice are typically resistant to experimental autoimmune encephalomyelitis (EAE) induced by MOG35-55 peptide.
- Murine cytomegalovirus (MCMV) is a common viral infection in mice.
Purpose of the Study:
- To investigate the effect of MCMV infection on EAE susceptibility in BALB/c mice.
- To elucidate the immunological mechanisms underlying MCMV-induced EAE.
Main Methods:
- Induction of EAE in BALB/c mice with MOG35-55 peptide before and after MCMV infection.
- Analysis of immune cell infiltrates (CD4+, CD8+) in the central nervous system.
- Ex vivo restimulation of CD8+ T cells with MOG35-55 peptide.
- Phenotypic analysis of dendritic cells and microglia.
- Assessment of Th1/Th17 cell differentiation.
Main Results:
- MCMV infection abrogated resistance to EAE in BALB/c mice, leading to clinical and histological signs similar to susceptible strains.
- CD8+ T cells constituted a significant portion of the inflammatory infiltrate, similar to multiple sclerosis.
- MCMV infection promoted a proinflammatory phenotype in dendritic cells and M1 microglia.
- Increased development of Th1/Th17 encephalitogenic cells was observed.
Conclusions:
- MCMV infection can overcome inherent resistance to EAE in BALB/c mice.
- The virus enhances autoimmune neuropathology by promoting proinflammatory antigen-presenting cells, Th1/Th17 responses, and CD8+ T cell reactivity to MOG35-55.
- These findings suggest a potential role for viral infections in exacerbating autoimmune neurological diseases.
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