The study of spontaneous autoimmunity in mouse models affords an opportunity to determine the cellular basis of the immune dysregulation observed in this disease. Recently, a new mouse strain, MRL/Mp-lpr/lpr (MRL/l) has been developed1 which carries an autosomal recessive gene (lpr) that results in massive lymph node enlargement concomitant with the development of several autoantibodies1-4. The interest in this strain lies in the possibility that the defect in T-cell regulation of the immune response is manifested at a different level from that in the NZB mouse3. It has been reported that the proliferating population of lymphoid cells in the nodes of these mice are T cells, but that many of them are devoid of Lyt surface antigens4. We have accordingly initiated several lines of research with these mice, including quantitative flow cytometry characterization of Lyt antigen expression of cells in the lymph nodes of the mice. In an approach to isolate and study the properties of these cells, we have also established continuous cell lines from the lymph node cells of MRL/l mice, using techniques similar to those used to establish continuous lines of antigen-activated cytotoxic T cells5,6 and helper T-cell populations7.
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