Interleukins in experimental autoimmune disease

New mouse models of SLE have been developed recently including strains bearing the lpr gene. The presence of this gene results in antibodies to nucleoproteins and DNA, immune complex glomerulonephritis, and proliferation of Lyt 1+23- T cells. A defect in Interleukin-2 (IL-2) production is a common abnormality in these autoimmune mice. We have utilized an antigen presentation system to study T cell proliferation in MRL/lpr, C57B16/lpr and C3H/He/lpr mice and their normal congenic counterparts. The normal mice proliferate well whereas there is little proliferation in the lpr variants. Mixing experiments demonstrate that the defect resides with the lpr responding T cells and not with the lpr macrophages. This abnormality could be due to defective IL-2 production by Lyt 1+23- T cells.