| First Author | Bachmann R | Year | 1999 |
| Journal | Am J Pathol | Volume | 154 |
| Issue | 5 | Pages | 1417-22 |
| PubMed ID | 10329594 | Mgi Jnum | J:114241 |
| Mgi Id | MGI:3688653 | Doi | 10.1016/S0002-9440(10)65395-3 |
| Citation | Bachmann R, et al. (1999) Impairment of TNF-receptor-1 signaling but not fas signaling diminishes T-cell apoptosis in myelin oligodendrocyte glycoprotein peptide-induced chronic demyelinating autoimmune encephalomyelitis in mice. Am J Pathol 154(5):1417-22 |
| abstractText | T-cell apoptosis in inflammatory demyelinating lesions of chronic myelin oligodendrocyte glycoprotein peptide35-55 induced autoimmune encephalomyelitis was studied in several different gene knockout mice as well as their wild-type counterparts. The gene deletions included tumor necrosis factor (TNF) alpha, lymphotoxin, TNF receptor 1 or 2, Fas-L, inducible nitric oxide synthase, perforin, and interleukin1beta-converting enzyme. Impairment of the TNF receptor 1 pathway led to a 50% reduction of T-cell apoptosis in the central nervous system lesions, whereas the other genetic deletions showed no significant effect. Our study thus identified the TNF receptor 1 signaling pathway as one mechanism responsible for the removal of T lymphocytes from inflammatory demyelinating lesions of the central nervous system. |
