Long-Evans Cinnamon (LEG) rats show a novel maturational arrest from C
D4(+)8(+) to CD4(+)8(-) thymocytes but a cause of this mutation is not
identified. The candidate for this mutation is a defect in the functi
on of CD4 or major histocompatibility complex (MHC) class II because g
ene-disrupted mice defective for CD4 or MHC class II molecules show a
specific defect in CD4(+) T cells. Previously, we showed that MHC clas
s II is not a cause of this maturational arrest. Therefore, in this st
udy, we focus on the function of CD4 molecules in LEC rat thymocytes.
CD4 molecules on LEC rat thymocytes associated with protein tyrosine k
inase, p56(kk), normally. Furthermore, cross-linking of CF4 molecules
by anti-rat CD4 mAb elicited the elevation of intracellular calcium co
ncentrations ([Ca2+](i)) in LEC rat thymocytes, suggesting that CD4 mo
lecules can deliver the signal normally. These results indicate that f
unction of CD4 is normal and the maturational blockade of CD4(+)8(-) t
hymocytes in LEC rats is not caused by specific lymphocyte molecules t
hat have been shown in gene-disrupted mice.