Abstract
Neuroadapted Sindbis virus infection of mice causes T cell-mediated fatal encephalomyelitis. In the absence of IL-10, pathogenic Th17 cells are increased and disease is accelerated. Lymphoid and myeloid cell contributions to IL-10 production were determined using VertX IL-10 transcriptional eGFP reporter mice. Effector and regulatory CD4(+) and CD8(+) T cells in the brain, but not the cervical lymph nodes, were the primary producers of IL-10. Th17 and Th1/Th17 cells were increased in mice that lacked T cell IL-10 production, although less than in the absence of IL-10. Morbidity and mortality were not affected suggesting an IL-10 threshold for disease exacerbation.
Keywords:
IL-10 source; Immunopathology; Mice; Sindbis virus; Th17.
Copyright © 2016 Elsevier B.V. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Alphavirus / pathogenicity
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Alphavirus Infections / genetics
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Alphavirus Infections / immunology*
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Alphavirus Infections / pathology*
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Animals
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Antigens, CD / metabolism
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Central Nervous System / pathology
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Central Nervous System / virology
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Disease Models, Animal
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Encephalomyelitis / genetics
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Encephalomyelitis / immunology*
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Encephalomyelitis / pathology*
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Encephalomyelitis / virology
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Flow Cytometry
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Gene Expression Regulation / drug effects
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Gene Expression Regulation / physiology
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Green Fluorescent Proteins / genetics
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Green Fluorescent Proteins / metabolism
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Interleukin-10 / genetics
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Interleukin-10 / metabolism*
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic
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Statistics, Nonparametric
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Th17 Cells / metabolism*
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Th17 Cells / pathology
Substances
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Antigens, CD
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IL10 protein, mouse
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enhanced green fluorescent protein
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Interleukin-10
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Green Fluorescent Proteins