期刊
JOURNAL OF IMMUNOLOGY
卷 190, 期 3, 页码 881-885出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1202925
关键词
-
类别
资金
- U.K. Medical Research Council [G0801924]
- Wellcome Trust [085399]
- Medical Research Council [G0801924, G0901697, G1100084] Funding Source: researchfish
- MRC [G0801924, G1100084, G0901697] Funding Source: UKRI
Mice lacking IL-6 are resistant to autoimmune diseases, such as experimental autoimmune encephalomyelitis (EAE), which is driven by CNS-reactive CD4(+) T cells. There are multiple cellular sources of IL-6, but the critical source in EAE has been uncertain. Using cell-specific IL-6 deficiency in models of EAE induced by active immunization, passive transfer, T cell transfer, and dendritic cell transfer, we show that neither the pathogenic T cells nor CNS-resident cells are required to produce IL-6. Instead, the requirement for IL-6 was restricted to the early stages of T cell activation and was entirely controlled by dendritic cell-derived IL-6. This reflected the loss of IL-6R expression by T cells over time. These data explain why blockade of IL-6R only achieves protection against EAE if used at the time of T cell priming. The implications for therapeutic manipulation of IL-6 signaling in human T cell-driven autoimmune conditions are considered. The Journal of Immunology, 2013, 190: 881-885.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据