Abstract
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 interactions. Conversely, adhesion of adult CD4+ CD45RA+ subpopulation to B cells is not regulated by ligands of CD4. We have investigated the regulation of adhesion of cord blood CD45RA^+^ CD4^+^ T lymphocytes. In contrast to adult CD45RA^+^ CD4^+^ T cells, cord blood CD45RA^+^ CD4^+^ T cells were strongly sensitive to the down‐regulation of adhesion mediated by the CD4‐HLA class II interaction, since adhesion to MHC class II(^+^) B cells was transient and inhibited by an anti‐CD4 antibody. In addition, human immunodeficiency virus gpl60, synthetic gpl06‐derived peptides encompassing a CD4 binding site inhibited conjugate formation between cord blood CD45RA^+^ CD4+ T cells and B cells. Following activation of the 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 occurred at day 8 following anti‐CD3 activation in correlation with a complete shift to a CD45RO phenotype of the cord blood CD4 T cells. These data suggest that CD4 T cell adhesion can be developmentally regulated.