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The Cellular and Genetic Basis of Murine Lupus

The pathogenesis of autoimmunity in New Zealand mice has been of great interest for a number of years. It has been thought that understanding the disease of NZB and (NZBXNZW) Fi mice should lead to understanding of a great variety of related diseases in several species, including man. Unfortunately, the search has, in general, been for a simple answer. Investigators have variously tried to implicate the thymus, T cell regulation, B cells, stem cells, thymic hormone, and a virus. All have been plausible, however the disease appears to be multifactorial (Steinberg et al. 1969), and no one factor has yet been able to explain all of the data. In the past few years, two new strains which develop lupus-like illnesses have been developed by Murphy and Roths (Murphy & Roths 1978). These have allowed for testing of hypotheses developed in the study of New Zealand mice. In addition, more sophisticated immune analysis has been applied to the study of the mice. Finally, genetic studies have been extended to include both recombinant inbred lines and the use of the C B A / N X-chromosome gene {Xid) as aids in improving our understanding of murine lupus. This review will emphasize the newer data developed in the past few years. We will try to indicate that, not only is murine lupus multifactorial, but that the cellular basis of illness may be different in different strains.