| First Author | Nose M | Year | 1998 |
| Journal | Int J Cardiol | Volume | 66 Suppl 1 |
| Pages | S37-41; discussion S43 | PubMed ID | 9951801 |
| Mgi Jnum | J:55587 | Mgi Id | MGI:1339001 |
| Doi | 10.1016/s0167-5273(98)00146-6 | Citation | Nose M, et al. (1998) Vasculitis-susceptible genes in mice with a deficit in Fas-mediated apoptosis. Int J Cardiol 66 Suppl 1:S37-41; discussion S43 |
| abstractText | Autoimmune diseases show complex pathological manifestations, which frequently involve systemic vasculitis. This complication is understood to be a manifestation of advanced disease, or to represent distinct entities, restricted by genetic and/or environmental factors. An MRL/Mp strain of mice bearing the Fas deletion mutant gene, lpr (MRL/lpr), spontaneously develop systemic vasculitis coincidentally with glomerulonephritis, arthritis and sialoadenitis, but a C3H/HeJ-lpr/lpr (C3H/lpr) strain does not. Thus, this is a suitable model for analyzing the genetic basis of vasculitis in autoimmune diseases. To genetically dissect these complex pathological manifestations, a linkage analysis of each lesion with polymorphic microsatellite markers was performed by using MRL/lpr x (MRL/lpr x C3H/lpr)F1 backcross mice. Vasculitis- susceptible gene loci were mapped on chromosomes 3 and 4, which were not associated with glomerulonephritis, arthritis and sialoadenitis. These results indicate that systemic vasculitis in MRL/lpr mice may be under the control of host genes which are different from those for other autoimmune diseases. |
