The murine gld mutation is targetted to the gene coding for the ligand of the Fas receptor for apoptosis. Gld mice display a lymphoproliferative and autoimmune syndrome that can be transferred in both irradiated euthymic wild and athymic beige (nubg) recipients. In order to test whether a supply of normal wild cells could correct the development of the gld syndrome, nubg mice were grafted with mixtures of gld and wild spleen cells from congenic donors which differed for the allotypes of the T-cell Thy1 membrane glycoprotein and/or of the B-cell Ig heavy chain. In the nubg chimeras, the wild spleen cells could down-regulate the hyperactivation of the B cells and the proliferation of the gld T cells, but this was not due to total eradication of the gld T-cell subset. Since this occurred in an athymic recipient, the correction of the gld syndrome did not require wild stem cell differentiation within a thymic environment, but should only depend on a sufficient Fas ligand supply by normal wild cells. Since the gld cells could proliferate in the nubg environment, the nubg environment could not provide sufficient Fas ligand to regulate the gld cell proliferation. Thus, the nubg B cells might lack Fas ligand expression, or express it but to a lower extent that T cells.