MRL/ I mice develop progressive, virulent autoilnmune disease that has many of the features of systemic lupus erythematosus. Prophylactic treatment of MRL/I mice with syngeneic photo inactivated autoimmune splenocytes improves survival and inhibits the fuhninant hyperproliferation of abnormal T cells and the production of high titer anti-DNA antibody invariably found in untreated mice. The proliferation of Thy 1 + splenic T cells was sigllificantly decreased, and prolonged T he MRL/ I mouse

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... l of systemic lupus erythematosus provides an experimental system that permits exploration of the effect ofT -cell directed therapcutic maneuvers on the course of autoimmune disease. MRL/ I mice develop lymphoid hyperplasia, B-ccll hypcracti vity, autoantibodies, circulating imlllune complexes, depressed serulll complement, thymic cortical atrophy [1,2], dermaritis [3 .4]. arthritis [S,6}. and fatal immune complex glomerulonephritis. The genome of the MRL/ l mouse contains the autosomal recess ive mutation Ipr. Homozygosity for this gene results in early onset of autoimmune disease with massive lymphadenopathy and splenomegaly duc to a proliferation of phenotypically aberrant 17-9}, functional inducer T cells [1 OJ. Initiation of autoimmune diseasc in these mice correlates with the onset ofT-ceil hyperproliferation. suggesting that the primary defect in this model relatcs in a misregulation of inducer T cells resulting in polyclonal B-cell stimulation. Therapies that ablate T cells can improve some of the parameters Manuscript