Limits...
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.

Show MeSH

Related in: MedlinePlus

Cytokine-pretreated endothelium increases CD54 expression on monocytes. The fluorescein isothiocyanate (FITC) mean fluorescence intensity (mfi) of monocytes that migrated through endothelium pretreated with tumour necrosis factor-α (TNF-α) (a) or interleukin-1α (IL-1α) (b) is compared with the mfi of monocytes that simultaneously migrated through untreated endothelium (control). Statistical significance: (a)P = 0.043; (b)P = 0.019.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC17829&req=5

Figure 4: Cytokine-pretreated endothelium increases CD54 expression on monocytes. The fluorescein isothiocyanate (FITC) mean fluorescence intensity (mfi) of monocytes that migrated through endothelium pretreated with tumour necrosis factor-α (TNF-α) (a) or interleukin-1α (IL-1α) (b) is compared with the mfi of monocytes that simultaneously migrated through untreated endothelium (control). Statistical significance: (a)P = 0.043; (b)P = 0.019.

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)

Cytokine-pretreated endothelium increases CD54 expression on monocytes. The fluorescein isothiocyanate (FITC) mean fluorescence intensity (mfi) of monocytes that migrated through endothelium pretreated with tumour necrosis factor-α (TNF-α) (a) or interleukin-1α (IL-1α) (b) is compared with the mfi of monocytes that simultaneously migrated through untreated endothelium (control). Statistical significance: (a)P = 0.043; (b)P = 0.019.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 4: Cytokine-pretreated endothelium increases CD54 expression on monocytes. The fluorescein isothiocyanate (FITC) mean fluorescence intensity (mfi) of monocytes that migrated through endothelium pretreated with tumour necrosis factor-α (TNF-α) (a) or interleukin-1α (IL-1α) (b) is compared with the mfi of monocytes that simultaneously migrated through untreated endothelium (control). Statistical significance: (a)P = 0.043; (b)P = 0.019.
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