The induction of EAE is only partially dependent on TNF receptor signaling but requires the IL-1 type I receptor
Copyright 2000 Academic Press.
| Veröffentlicht in: | Clinical immunology (Orlando, Fla.). - 1999. - 95(2000), 2 vom: 01. Mai, Seite 117-23 |
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| 1. Verfasser: | |
| Weitere Verfasser: | , , , , |
| Format: | Aufsatz |
| Sprache: | English |
| Veröffentlicht: |
2000
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| Zugriff auf das übergeordnete Werk: | Clinical immunology (Orlando, Fla.) |
| Schlagworte: | Journal Article Research Support, U.S. Gov't, P.H.S. Receptors, Interleukin-1 Receptors, Tumor Necrosis Factor |
| Zusammenfassung: | Copyright 2000 Academic Press. Experimental autoimmune encephalomyelitis develops in mice immunized with CNS antigens. To elucidate the role that specific proinflammatory cytokines play in the induction of this process we examined the development of EAE in mice with targeted disruptions of the TNF p55 or p75 or the IL-1 p80 receptors. EAE developed in mice with either one or both TNF receptors deleted although the onset of disease in mice with the p55 receptor deleted was delayed. However, mice with a deletion of the IL-1 p80 receptor failed to develop any inflammatory lesions in the CNS or evidence of clinical EAE. Thus we conclude that TNF or its receptors contribute to, but are not necessary for, the induction of EAE while the IL-1 p80 receptor is absolutely required. The p55 TNF receptor plays a role in determining the onset of disease and its severity |
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| Beschreibung: | Date Completed 16.06.2000 Date Revised 14.11.2007 published: Print Citation Status MEDLINE |
| ISSN: | 1521-7035 |