Similar to the traditional New Zealand models, the (NZB x SWR) F1 (SNF1) model has been often used to characterize the anti-DNA response, including the recognition of nucleosomal peptides by autoreactive T cells (60,62,177), as well as the importance of specific residues and motifs in anti-DNA antibodies (57), often in "receptor presentation" (178). Some genetic studies have begun (179,180), and as in NZ strains, some studies have confirmed potential roles for peptide tolerization (61) and costimulatory blockade (181).
The (NZW x BXSB) F1 model resembles the traditional BXSB model in several respects, including the dominant importance of Yaa (182). Interestingly, however, these animals develop glomerulonephritis in both sexes (resembling BXSB in males, NZB x NZW F1's in females), as well as immune-mediated thrombocytopenic purpura, degenerative vascular lesions, and coronary artery disease, which may be related to anticardiolipin antibodies (183-187). Still, few studies to date have directly investigated pathogenic processes in this model, with only a few preliminary genetic studies involving MHC and other loci (188,189).
Other, even less-well-characterized models include the NZW (female) x SB/ Le (male) F1, which develops disease virtually identical to BXSB (160), and the experimental autoimmune encephalomyelitis-susceptible SWR x SJL F1, which develops several autoantibodies and glomerulonephritis similar to human SLE (190,191). The spontaneous crescentic glomerulonephritis-forming mouse/ Kinjoh (SCG/Kj) was derived from a BXSB/Mp x MRL/Mp-lpr/lpr F1 hybrid (192) and interestingly develops antineutrophil cytoplasmic antibodies that crossreact with anti-DNA (193).
Was this article helpful?