Angiopoietin-2 promotes myeloid cell infiltration in a β2- integrin-dependent manner

Alexander Scholz, Victoria Lang, Reinhard Henschler, Marcus Czabanka, Peter Vajkoczy, Emmanouil Chavakis, Janina Drynski, Patrick N. Harter, Michel Mittelbronn, Daniel J. Dumont, Karl H. Plate, Yvonne Reiss*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

74 Citations (Scopus)


In human inflammatory diseases, we identified endothelial angiopoietin-2 (Ang-2) expression to be strongly associated with inflammations mediated by myeloid cells but not lymphocytes. To identify the underlying mechanism, we made use of a transgenic mouse model with inducible endothelial cell-specific expression of Ang-2. In this model, in the absence of inflammatory stimuli, long-term expression of Ang-2 led to a time-dependent accumulation of myeloid cells in numerous organs, suggesting that Ang-2 is sufficient to recruit myeloid cells. In models of acute inflammation, such as delayed-type hypersensitivity and peritonitis, Ang-2 transgenic animals showed an increased responsiveness. Intravital fluorescence video microscopy revealed augmented cell adhesion as an underlying event. Consequently, we demonstrated that Ang-2 is able to induce strong monocyte adhesion under shear in vitro, which could be blocked by antibodies to β2-integrin. Taken together, our results describe Ang-2 as a novel, endothelialderived regulator of myeloid cell infiltration that modulates β2-integrin-mediated adhesion in a paracrine manner.

Original languageEnglish
Pages (from-to)5050-5059
Number of pages10
Issue number18
Publication statusPublished - 3 Nov 2011
Externally publishedYes


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