EAE mediated by a non-IFN-Γ/non-IL-17 pathway
dc.contributor.author | Kroenke, Mark A. | en_US |
dc.contributor.author | Chensue, Stephen W. | en_US |
dc.contributor.author | Segal, Benjamin M. | en_US |
dc.date.accessioned | 2010-09-02T15:21:44Z | |
dc.date.available | 2011-03-01T16:26:45Z | en_US |
dc.date.issued | 2010-08 | en_US |
dc.identifier.citation | Kroenke, Mark A.; Chensue, Stephen W.; Segal, Benjamin M. (2010). "EAE mediated by a non-IFN-Γ/non-IL-17 pathway." European Journal of Immunology 40(8): 2340-2348. <http://hdl.handle.net/2027.42/77956> | en_US |
dc.identifier.issn | 0014-2980 | en_US |
dc.identifier.issn | 1521-4141 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/77956 | |
dc.description.abstract | 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. | en_US |
dc.format.extent | 435625 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | WILEY-VCH Verlag | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Microbiology and Immunology | en_US |
dc.title | EAE mediated by a non-IFN-Γ/non-IL-17 pathway | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Biological Chemistry | en_US |
dc.subject.hlbsecondlevel | Public Health | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Holtom-Garrett Program in Neuroimmunology, Department of Neurology, University of Michigan, Ann Arbor, MI, USA ; Department of Microbiology and Immunology, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA | en_US |
dc.contributor.affiliationum | Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA ; Department of Pathology and Laboratory Medicine, VA Ann Arbor Healthcare System, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationum | Holtom-Garrett Program in Neuroimmunology, Department of Neurology, University of Michigan, Ann Arbor, MI, USA ; Department of Neurology, 4013 BSRB, 109 Zina Pitcher Place, Ann Arbor, MI 48109, USA Fax:+1-734-615-7300 | en_US |
dc.identifier.pmid | 20540117 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/77956/1/2340_ftp.pdf | |
dc.identifier.doi | 10.1002/eji.201040489 | en_US |
dc.identifier.source | European Journal of Immunology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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