The survival of patients with systemic lupus erythematosus (SLE) has improved tremendously over the past several decades, from a two year survival of 50% in 1939¹ to five and 10 year survival of 90% and 80% respectively in the 1980s.2 This improvement is attributed mainly to the availability of dialysis, use of corticosteroids and cytotoxic drugs, and improved antibiotics and antihypertensive agents. However, since the introduction of cytotoxic agents in the treatment of severe SLE, no significant breakthrough in the treatment of lupus patients has been reported. This is probably because the aetiology of the disease is still unknown, and because of the great diversity of the clinical expressions of the disease—which makes it difficult to assess the effect of novel treatments—and the long follow up needed to evaluate changes in prognosis. Moreover, since 80-90% of lupus patients are young women, the use of experimental treatments which might decrease fertility, increase teratogenesis, or have other undesirable side effects is greatly curtailed. Because of these limitations, animal models of SLE could be of considerable value in the evaluation of novel and experimental treatments which that cannot be tested directly on patients. Various animal models of human SLE have been described, which tend to reflect different aspects of the disease. The prototype murine model of spontaneous SLE is the New Zealand black (NZB) mouse,3 principally a model of autoimmune haemolytic anaemia, accompanied by kidney disease and autoantibodies against erythrocytes, ssDNA and dsDNA. A hybrid strain derived from the NZB mouse is one produced by mating this strain with the New Zealand white mouse, the offspring being known as (NZB×NZW)F₁.3 The MRL/lpr mouse strain is a model for an accelerated membranoproliferative glomerulo-nephritis associated with anti-DNA production.4 Additional clinical features include lymphoproliferation, synovitis, and vasculitis. Another mouse …