scispace - formally typeset
N

Nico van Rooijen

Researcher at VU University Amsterdam

Publications -  514
Citations -  69830

Nico van Rooijen is an academic researcher from VU University Amsterdam. The author has contributed to research in topics: Inflammation & Immune system. The author has an hindex of 130, co-authored 513 publications receiving 62623 citations. Previous affiliations of Nico van Rooijen include Vanderbilt University Medical Center & Walter and Eliza Hall Institute of Medical Research.

Papers
More filters
Journal ArticleDOI

Inflammatory monocytes recruited after skeletal muscle injury switch into antiinflammatory macrophages to support myogenesis

TL;DR: In conclusion, injured skeletal muscle recruits monocyte (MO) exhibiting inflammatory profiles that operate phagocytosis and rapidly convert to antiinflammatory MPs that stimulate myogenesis and fiber growth.
Journal ArticleDOI

CD47 is an adverse prognostic factor and therapeutic antibody target on human acute myeloid leukemia stem cells.

TL;DR: It is found that increased CD47 expression is an independent, poor prognostic factor that can be targeted on human AML stem cells with blocking monoclonal antibodies capable of enabling phagocytosis of LSC.
Journal ArticleDOI

Local Macrophage Proliferation, Rather than Recruitment from the Blood, Is a Signature of TH2 Inflammation

TL;DR: It is revealed that a distinct process exists in which tissue macrophages undergo rapid in situ proliferation in order to increase population density, and expansion of innate cells necessary for pathogen control or wound repair can occur without recruitment of potentially tissue-destructive inflammatory cells.
Journal ArticleDOI

Monocyte subsets differentially employ CCR2, CCR5, and CX3CR1 to accumulate within atherosclerotic plaques

TL;DR: Analyzing mouse monocyte subsets in apoE-deficient mice and tracing their differentiation and chemokine receptor usage as they accumulated within atherosclerotic plaques suggests antagonizing CX3CR1 may be effective therapeutically in ameliorating CCR2(+) monocyte recruitment to plaques without impairing their C CR2-dependent responses to inflammation overall.