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Arthritis Research and Therapy

, 3:127

First Online: 11 January 2001Received: 06 August 2000Revised: 23 November 2000Accepted: 14 December 2000


In our study we characterised the immunophenotype of monocytes that migrated through an endothelial cell EC monolayer in vitro. We found that monocyte migration led to an enhanced expression of CD11a, CD33, CD45RO, CD54 intercellular cell-adhesion molecule ICAM-1 and human leucocyte antigen-DR. The most striking increase was observed for ICAM-1 when ECs were activated with tumour necrosis factor-α and interleukin-1α. The results of our study indicate the following: 1 there is a characteristic immunophenotype on the surface of monocytes after transendothelial migration; 2 this 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 activating ECs is sufficient to enhance monocyte migration and that this, in turn, can induce changes consistent with an activated phenotype known to be interactive between antigen-presenting cells and T cells. These results have implications for our pathogenetic insights into rheumatoid arthritis.

Keywordsendothelium inflammation migration monocyte transendothelial migration AbbreviationsAPC= antigen-presenting cell

BND= population of cells bound to the surface

EC= endothelial cell

ICAM= intercellular cell-adhesion molecule

IFN-γ= interferon-γ

IL= interleukin

MIG= population of cells migrated into collagen gel

MIP= macrophage inflammatory protein

NAD= non-adherentcell population

PBMC= peripheral blood mononuclear cells

PBS= phosphate-buffered saline

RA= rheumatoid arthritis

TNF-α=tumour necrosis factor-α.

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Autor: Johannes Grisar - Philipp Hahn - Susanne Brosch - Meinrad Peterlik - Josef S Smolen - Peter Pietschmann


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