| First Author | Zhou T | Year | 1996 |
| Journal | J Immunol | Volume | 156 |
| Issue | 8 | Pages | 2661-5 |
| PubMed ID | 8609380 | Mgi Jnum | J:32463 |
| Mgi Id | MGI:79959 | Doi | 10.4049/jimmunol.156.8.2661 |
| Citation | Zhou T, et al. (1996) Greatly accelerated lymphadenopathy and autoimmune disease in lpr mice lacking tumor necrosis factor receptor I. J Immunol 156(8):2661-5 |
| abstractText | Fas and TNF receptor I (TNF-RI) share homology at their cytoplasmic death domain and belong to the same gene family, but utilize different pathways to signal activation-induced cell death. To determine the combined effects of defective TNF-RI and Fas signaling on lymphadenopathy and autoimmune disease, we backcrossed TNF-RI knockout mice (Tnfr1(0/0)) with Fas-deficient C57BL/6-lpr/lpr mice. Tnfr1(0/0)lpr/lpr mice developed greatly accelerated lymphadenopathy and autoantibody production compared with C57BL/6-lpr/ lpr mice. Tnfr1(0/0)-lpr/lpr mice also exhibited high mortality and early onset autoimmune disease characterized by massive mononuclear cell infiltration in liver, kidney, lung, and knee joints. These results indicate that the Fas-mediated apoptosis defect in lpr mice is accelerated in the absence of TNF-RI and that normal expression of TNF-RI might partially compensate for the Fas-mediated apoptosis defect of mononuclear cells in lpr mice. |
