ArticleProceedings of the National Academy of Sciences of the United States of America2014
Interleukin 10 modulation of pathogenic Th17 cells during fatal alphavirus encephalomyelitis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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48 citing papers in PubMed, 73 citations in OpenAlex.
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- Unraveling the complex interplay: immunopathology and immune evasion strategies of alphaviruses with emphasis on neurological implications.Frontiers in cellular and infection microbiology · 2024Review
- An important call: Suggestion of using IL-10 as therapeutic agent for COVID-19 with ARDS and other complications.Virulence · 2023Review
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- Antiviral activity of glucosylceramide synthase inhibitors in alphavirus infection of the central nervous system.Brain communications · 2023Article
- Paradoxical roles for programmed cell death signaling during viral infection of the central nervous system.Current opinion in neurobiology · 2022Review
- Effect of IL-10 Deficiency on TGFβ Expression during Fatal Alphavirus Encephalomyelitis in C57Bl/6 Mice.Viruses · 2022Article
- Interleukin-17 contributes to Ross River virus-induced arthritis and myositis.PLoS pathogens · 2022Article
- Curdlan, a Microbial β-Glucan, Has Contrasting Effects on Autoimmune and Viral Models of Multiple Sclerosis.Frontiers in cellular and infection microbiology · 2022Article
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- The NF-κB/leukemia inhibitory factor/STAT3 signaling pathway in antibody-mediated suppression of Sindbis virus replication in neurons.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Innate immune response in neuronopathic forms of Gaucher disease confers resistance against viral-induced encephalitis.Acta neuropathologica communications · 2020Article
- Interferon-Gamma Modulation of the Local T Cell Response to Alphavirus Encephalomyelitis.Viruses · 2020Article
- Molecular switches for regulating the differentiation of inflammatory and IL-10-producing anti-inflammatory T-helper cells.Cellular and molecular life sciences : CMLS · 2020Review
- Immunopathogenesis of alphaviruses.Advances in virus research · 2020Article
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4 authors at 1 institution in 1 country.
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Abstract
Mosquito-borne alphaviruses are important causes of epidemic encephalomyelitis. Neuronal cell death during fatal alphavirus encephalomyelitis is immune-mediated; however, the types of cells involved and their regulation have not been determined. We show that the virus-induced inflammatory response was accompanied by production of the regulatory cytokine IL-10, and in the absence of IL-10, paralytic disease occurred earlier and mice died faster. To determine the reason for accelerated disease in the absence of IL-10, immune responses in the CNS of IL-10(-/-) and wild-type (WT) mice were compared. There were no differences in the amounts of brain inflammation or peak virus replication; however, IL-10(-/-) animals had accelerated and increased infiltration of CD4(+)IL-17A(+) and CD4(+)IL-17A(+)IFNγ(+) cells compared with WT animals. Th17 cells infiltrating the brain demonstrated a pathogenic phenotype with the expression of the transcription factor, Tbet, and the production of granzyme B, IL-22, and GM-CSF, with greater production of GM-CSF in IL-10(-/-) mice. Therefore, in fatal alphavirus encephalomyelitis, pathogenic Th17 cells enter the CNS at the onset of neurologic disease and, in the absence of IL-10, appear earlier, develop into Th1/Th17 cells more often, and have greater production of GM-CSF. This study demonstrates a role for pathogenic Th17 cells in fatal viral encephalitis.
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