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

Kirsten A Kulcsar1, Diane E Griffin1

  • 1Program in Cellular and Molecular Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA; W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, 21205, USA.

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.

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