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Phenotypic characteristics of human monocytes undergoing transendothelial migration.

Grisar J, Hahn P, Brosch S, Peterlik M, Smolen JS, Pietschmann P - Arthritis Res. (2001)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Division of Rheumatology, Department of Internal Medicine III, University of Vienna, Währinger Gürtel 18-20, A-1180 Vienna, Austria. johannes.grisar@akh-wien.ac.at

ABSTRACT
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-alpha and interleukin-1alpha. 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.

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Migration through endothelium increases CD54 expression on monocytes. Histograms show the CD54 mean fluorescence intensity (mfi) of monocytes that migrated through untreated endothelium (grey line in each panel), or endothelium pretreated with tumour necrosis factor-α (black line in middle panel) or interleukin-1α (black line in bottom panel). CD54 mfi of the nonadherent monocyte fraction is shown by a dotted line (top panel), isotype controls are shown by a thin black line in each panel. The experiment shown is representative of three independent experiments.
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Figure 3: Migration through endothelium increases CD54 expression on monocytes. Histograms show the CD54 mean fluorescence intensity (mfi) of monocytes that migrated through untreated endothelium (grey line in each panel), or endothelium pretreated with tumour necrosis factor-α (black line in middle panel) or interleukin-1α (black line in bottom panel). CD54 mfi of the nonadherent monocyte fraction is shown by a dotted line (top panel), isotype controls are shown by a thin black line in each panel. The experiment shown is representative of three independent experiments.

Mentions: Pretreatment of ECs with TNF-α led to a significant decrease in CD45RO and HLA-DR on migrated monocytes. In contrast, CD54 (ICAM-1) was significantly increased on monocytes that migrated through endothelium pretreated with TNF-α or IL-1α in comparison with migration through untreated endothelium (Figs 3 and 4, Table 3).


Phenotypic characteristics of human monocytes undergoing transendothelial migration.

Grisar J, Hahn P, Brosch S, Peterlik M, Smolen JS, Pietschmann P - Arthritis Res. (2001)

Migration through endothelium increases CD54 expression on monocytes. Histograms show the CD54 mean fluorescence intensity (mfi) of monocytes that migrated through untreated endothelium (grey line in each panel), or endothelium pretreated with tumour necrosis factor-α (black line in middle panel) or interleukin-1α (black line in bottom panel). CD54 mfi of the nonadherent monocyte fraction is shown by a dotted line (top panel), isotype controls are shown by a thin black line in each panel. The experiment shown is representative of three independent experiments.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC17829&req=5

Figure 3: Migration through endothelium increases CD54 expression on monocytes. Histograms show the CD54 mean fluorescence intensity (mfi) of monocytes that migrated through untreated endothelium (grey line in each panel), or endothelium pretreated with tumour necrosis factor-α (black line in middle panel) or interleukin-1α (black line in bottom panel). CD54 mfi of the nonadherent monocyte fraction is shown by a dotted line (top panel), isotype controls are shown by a thin black line in each panel. The experiment shown is representative of three independent experiments.
Mentions: Pretreatment of ECs with TNF-α led to a significant decrease in CD45RO and HLA-DR on migrated monocytes. In contrast, CD54 (ICAM-1) was significantly increased on monocytes that migrated through endothelium pretreated with TNF-α or IL-1α in comparison with migration through untreated endothelium (Figs 3 and 4, Table 3).

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Division of Rheumatology, Department of Internal Medicine III, University of Vienna, Währinger Gürtel 18-20, A-1180 Vienna, Austria. johannes.grisar@akh-wien.ac.at

ABSTRACT
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-alpha and interleukin-1alpha. 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.

Show MeSH
Related in: MedlinePlus