T cell-derived interleukin-10 is an important regulator of the Th17 response during lethal alphavirus encephalomyelitis
T cell-derived interleukin-10 is an important regulator of the Th17 response during lethal alphavirus encephalomyelitis
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DOI：
10.1016/j.jneuroim.2016.04.010
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发表时间：
2016-06-15
影响因子：
3.3
通讯作者：
Griffin, Diane E.
中科院分区：
文献类型：
--
作者：
Kulcsar, Kirsten A.;Griffin, Diane E.
神经适应性Sindbis病毒感染小鼠引起T细胞介导的致死性脑脊髓炎。在缺乏IL - 10的情况下，致病性Th17细胞增加，疾病加速。使用VertX IL-10转录eGFP报告小鼠来测定淋巴细胞和髓细胞对IL-10产生的贡献。脑内的效应性和调节性CD4（+）和CD8(+) T细胞是IL-10的主要产生细胞，而不是颈部淋巴结。在缺乏T细胞IL-10产生的小鼠中，Th17和Th1/Th17细胞增加，尽管低于缺乏IL-10的小鼠。发病率和死亡率未受影响，提示存在IL-10疾病恶化阈值。(C) 2016 Elsevier B.V.版权所有
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. (C) 2016 Elsevier B.V. All rights reserved.