In our study we characterised the immunophenotype of monocytes that migrate
d through an endothelial cell (EC) monolayer in vitro. We found that monocy
te migration led to an enhanced expression of CD11a, CD33, CD45RO, CD54 [in
tercellular cell-adhesion molecule (ICAM)-1] and human leucocyte antigen-DR
. The most striking increase was observed for ICAM-1 when ECs were activate
d with tumour necrosis factor-alpha and interleukin-1 alpha. The results of
our study indicate the following: (1) there is a characteristic immunophen
otype on the surface of monocytes after transendothelial migration; (2) thi
s phenotype seems to be induced by interactions between monocytes and ECs;
and (3) this change is enhanced by the pretreatment of ECs with cytokines.
Taken together, the results suggest that local cytokine production activati
ng ECs is sufficient to enhance monocyte migration acid that this, in turn,
can induce changes consistent with an activated phenotype known to be inte
ractive between antigen-presenting cells and T cells. These results have im
plications for our pathogenetic insights into rheumatoid arthritis.