The murine gld mutation is targetted to the gene coding for the ligand
of the Fas receptor for apoptosis. Gld mice display a lymphoprolifera
tive and autoimmune syndrome that can be transferred in both irradiate
d 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 wil
d spleen cells from congenic donors which differed for the allotypes o
f the T-cell Thyl 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 su
bset. Since this occurred in an athymic recipient, the correction of t
he gld syndrome did not require wild stem cell differentiation within
a thymic environment, but should only depend on a sufficient Fas ligan
d supply by normal wild cells. Since the gld cells could proliferate i
n the nubg environment, the nubg environment could not provide suffici
ent 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.