EAE mediated by a non-IFN-γ/non-IL-17 pathway.
EAE mediated by a non-IFN-γ/non-IL-17 pathway.
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DOI：
10.1002/eji.201040489
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发表时间：
2010-08
影响因子：
5.4
通讯作者：
Segal, Benjamin M.
中科院分区：
文献类型：
--
作者：
Kroenke, Mark A.;Chensue, Stephen W.;Segal, Benjamin M.
Previous studies have shown that EAE can be elicited by the adoptive transfer of either IFN-γ-producing (Th1) or IL-17-producing (Th17) myelin-specific CD4+ T-cell lines. Paradoxically, mice deficient in either IFN-γ or IL-17 remain susceptible to EAE following immunization with myelin antigens in CFA. These observations raise questions about the redundancy of IFN-γ and IL-17 in autoimmune demyelinating disease mediated by a diverse, polyclonal population of autoreactive T cells. In this study, we show that an atypical form of EAE, induced in C57BL/6 mice by the adoptive transfer of IFN-γ-deficient effector T cells, required IL-17 signaling for the development of brainstem infiltrates. In contrast, classical EAE, characterized by predominant spinal cord inflammation, occurred in the combined absence of IFN-γ and IL-17 signaling, but was dependent on GM-CSF and CXCR2. Our findings contribute to a growing body of data, indicating that individual cytokines vary in their importance across different models of CNS autoimmunity.
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影响因子：
15.9
作者：
Haak, Stefan;Croxford, Andrew L.;Waisman, Ari
通讯作者：
Waisman, Ari
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DOI：
10.1084/jem.177.6.1699
发表时间：
1993-06-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Bikoff EK;Huang LY;Episkopou V;van Meerwijk J;Germain RN;Robertson EJ
通讯作者：
Robertson EJ
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影响因子：
15.3
作者：
Bettelli, E;Sullivan, B;Szabo, SJ;Sobel, RA;Glimcher, H;Kuchroo, VK
通讯作者：
Kuchroo, VK
DOI：
10.1084/jem.20071119
发表时间：
2008-09-29
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Sonderegger I;Iezzi G;Maier R;Schmitz N;Kurrer M;Kopf M
通讯作者：
Kopf M
影响因子：
5.8
作者：
Matusevicius, D;Kivisäkk, P;Link, H
通讯作者：
Link, H