Our earlier studies showed that although CD27 was stably expressed on
the CD45RA(+)-CD45RO(-)CD29(low) subset of CD4 T cells, its expression
on the CD45RA(-)CD45RO(+)CD29(high) subset of CD4 T cells was gradual
ly lost within 3 weeks after PHA activation. In the present study, we
further determined the mechanisms by which the CD27 expression was dif
ferentially regulated on the subsets of CD4 T cells. We showed that di
sappearance of CD27 from the surface of the CD45RA(-)CD45RO(+) subset
of CD4 T cells was not solely due to the shedding of the CD27 molecule
from the cell surface since the release of a soluble form fo the CD27
molecule from the CD45RO(+) CD4 T cells was consistently less than th
at from CD45RA(+) CD4 T cells. Although the surface CD27 expression wa
s undetectable on long-term cultured T cell lines originally derived f
rom CD45RO(+) CD4 T cells, some of these cells still expressed intrace
llular CD27 and CD27 mRNA. Moreover, restimulation could not induce CD
27 expression on such cells. Further analysis of CD27 protein and mRNA
expression at a clonal level showed that cloned cells derived from CD
45RO(+) CD4 T cells having lost cell surface expression of CD27 were o
f two types: one expressed intracellular CD27 mRNA and protein whereas
the second lacked both intracellular CD27 mRNA and protein. (C) 1994
Academic Press, Inc.