C57B1/6 mice homozygous at the lpr (lymphoproliferation) locus display evident lymphadenopathy (in our B6 colony, primordially cervical lymph node enlargement) and autoimmunity (various autoantibodies). Four groups of mice corresponding to the diverse combinations of the lpr gene and the nu (nude, athymic) gene on the B6 genetic background have been compared for signs of lymphadenopathy. It occurred in all tested B6 +/+, lpr/lpr mice and none of the other groups (B6 nu/nu, +/+; B6 nu/nu, lpr/lpr and B6 +/+, +/+). B cell hyperactivity/autoimmunity was also evaluated by serum antibody analyses: higher serum immunoglobulin levels, anti-nuclear antibodies, anti-native DNA, anti-single stranded DNA, rheumatoid-like factors (anti-rabbit IgG), and natural antibodies against dinitrophenol and trinitrophenol haptens and their non cross reactive carriers: bovine serum albumin, hen egg albumin and keyhole limpet haemocyanin. Interestingly the levels of serum immunoglobulins and of some specific antibodies were somewhat higher in B6 nu/nu, lpr/lpr than in 'normal' B6 nu/nu, +/+, though they remained much lower than in B6 +/+, lpr/lpr animals. This suggests that the lpr gene may express its influence on the level of B cell activity in the absence of T lineage cells that would have normally matured in a thymus and that this effect of the lpr gene does not require the massive proliferation of T lineage cells observed in B6 +/+, lpr/lpr mice.