It is well known that chronic graft-vs-host (GVH) disease in mice has similarities to human SLE, and several models have been used for these investigations. The GVH model offers significant advantages over the existing, spontaneous SLE-prone mice in that it can be reliably induced and it follows a predictable, relatively short time course. Gleichmann and associates successfully induced a syndrome strongly resembling SLE in a suitable chronic GVH disease made in nonirradiated, H-2-incompati-ble (C57BL/10 x DBA/2)F1 mice injected intravenously with DBA/2 spleen cells and lymph node cells (Gleichmann et al. 1982, Van Rappard-Van Der Veen et al. 1983). Their model develops subepidermal immunoglobulin deposits like inbred SLE-prone mice. (BALB/c x A/J)F1 mice inoculated with A/J lymphocytes show mixed connective tissue disease-like symptoms, including finger swelling, alopecia, and proteinuria (Gelpi et al. 1988). Because chronic GVH models for SLE are useful for investigating cellular-level immune abnormalities, it is likely that the effects and mechanisms of immunosuppressive drugs or therapy can be investigated more precisely in GVH models than in inbred mouse models (Appleby et al. 1989). The 8-methoxypsoralen and UVA light treatment of DBA/2 cells can vaccinate recipient mice against the progression of GVH reaction-initiated SLE-like disease by using the same GVH disease system (Girardi et al. 1995). Anti-a0TCR monoclonal antibody is also effective as a therapeutic agent (Maeda and Nomoto 1995).
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