Mice bearing the non-allelic autosomal recessive mutations, lpr and gld, exhibit many abnormalities in common. All mouse stains homozygous for either of these mutations develop lymphadenopathy, splenomegaly, and autoimmunity of varying severity. These abnormalities appear to be due to expansion of an unusual subset of T cells. Methods were designed to specifically purify the abnormal T cells from mice with either mutation. The abnormal cells were shown to be of T cell origin and to express the T cell receptor on their surfaces. By a variety of criteria, the abnormal T cells from mice with either mutation were shown to be identical. In addition, an unusual intrinsic phosphorylation of a 21 KD protein was shared by the abnormal cells characteristic of both mutations. These findings reinforce the suggestion that lpr and gld may affect different enzymes in a common metabolic pathway of central importance to T cell function.
