Antigen-independent adhesion of resting adult CD4+ CD45RO+ T cells to
B lymphocytes has been shown to be transient and can be down-regulated
by CD4 major histocompatibility complex (MHC) class II molecule inter
actions. Conversely, adhesion of adult CD4+ CD45RA+ subpopulation to B
cells is not regulated by ligands of CD4. We have investigated the re
gulation of adhesion of cord blood CD45RA+ CD4+ T lymphocytes. In cont
rast to adult CD45RA+ CD4+ T cells, cord blood CD45RA+ CD4+ T cells we
re strongly sensitive to the down-regulation of adhesion mediated by t
he CD4-HLA class II interaction, since adhesion to MHC class II(+) B c
ells was transient and inhibited by an anti-CD4 antibody. In addition,
human immunodeficiency virus gp160, synthetic gp106-derived peptides
encompassing a CD4 binding site inhibited conjugate formation between
cord blood CD45RA+ CD4+ T cells and B cells. Following activation of t
he cord blood CD4 T cells by an anti-CD3 antibody, a conversion from a
transient to a stable adhesion pattern of cord blood CD4 T cells to B
cells occurred in 2 days. The reversal to a transient adhesion occurr
ed at day 8 following anti-CD3 activation in correlation with a comple
te shift to a CD45RO phenotype of the cord blood CD4 T cells. These da
ta suggest that CD4 T cell adhesion can be developmentally regulated.