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

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.

journal_name

J Neuroimmunol

journal_title

Journal of neuroimmunology

authors

Kulcsar KA,Griffin DE

doi

10.1016/j.jneuroim.2016.04.010

subject

Has Abstract

pub_date

2016-06-15 00:00:00

pages

60-7

eissn

0165-5728

issn

1872-8421

pii

S0165-5728(16)30080-7

journal_volume

295-296

pub_type

杂志文章

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