Homozygosity for either the lymphoproliferation (lpr) or the generalized lymphoproliferative disease (gld) mutation of mice causes the development of strikingly similar autoimmune and lymphoproliferative syndromes. The relationship between thelprandgldmutations was studied by grafting B6gldspleen cells (SC) to athymic B6nude lprmice (B6nulpr)or to B6nude(B6nu)mice as controls. The injection of B6gldSC, but not of B6wildSC, to B6nulprmice caused a prolongation of survival of the short living B6nulprrecipients. This was associated with elevated anti-single stranded DNA antibody titers and a serum hyperglobulin-emia, as well as by a splenomegaly which was nearly as high as in genetically B6gldmice, and by a marked lymphadenopathy (though milder than that of B6gldmice). In contrast the[gldnu]chimaeras showed a more attenuated form ofgld-inducedsyndrome. These results suggest that thelprenvironment supplied in athymiclprrecipients is compatible with-and may even favour-the development of the gld-induced syndrome.