| First Author | Eugster HP | Year | 1999 |
| Journal | Eur J Immunol | Volume | 29 |
| Issue | 2 | Pages | 626-32 |
| PubMed ID | 10064079 | Mgi Jnum | J:115225 |
| Mgi Id | MGI:3691156 | Doi | 10.1002/(SICI)1521-4141(199902)29:02<626::AID-IMMU626>3.0.CO;2-A |
| Citation | Eugster HP, et al. (1999) Severity of symptoms and demyelination in MOG-induced EAE depends on TNFR1. Eur J Immunol 29(2):626-32 |
| abstractText | The individual role of tumor necrosis factor receptor 1 (TNFR1) and TNFR2 signaling in experimental autoimmune encephalomeylitis (EAE) was investigated using mice lacking TNFR1 (TNFR1-/-), TNFR2 (TNFR2-/-) as well as double receptor (TNFR1/2-/-) and double ligand (TNF/LT alpha-/-) knockout mice. In wild-type (wt) mice immunized with myelin oligodendrocyte glycoprotein (MOG) peptide 35-55 the clinical course is characterized by an acute disease onset with peak disease scores and a consecutive chronic phase lasting up to 60 days. Compared to control mice, TNF/LT alpha-deficient mice showed a significant delay in disease onset and a remarkable reduction in demyelination which was, however, associated with increased inflammation. In TNFR1-/- and TNFR1/2-/- mice, the disease course was comparable to TNF/LT alpha-deficient mice but rather monophasic and less severe at late time points. Likewise only minimal spinal cord demyelination became apparent. In contrast, the course of EAE in TNFR2-/- mice was severe and associated with remarkable demyelination. Taken together these findings define TNFR1 as crucial mediator in MOG-induced EAE and suggest a protective role for TNFR2 signaling in the clinical course of EAE. |
