T cell-derived interleukin-10 is an important regulator of the Th17 response during lethal alphavirus encephalomyelitis

Kirsten A. Kulcsar, Diane E. Griffin

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)60-67
Number of pages8
JournalJournal of Neuroimmunology
Volume295-296
DOIs
StatePublished - Jun 15 2016

Keywords

  • IL-10 source
  • Immunopathology
  • Mice
  • Sindbis virus
  • Th17

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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