Ine M. J. Wolfs

High-Density Lipoproteins Exert Pro-inflammatory Effects on Macrophages via Passive Cholesterol Depletion and PKC-NF-κB/STAT1-IRF1 Signaling.

Kimberly R. McDaniels, L. Touqui, T. Lawrence, 2017, Cell metabolism.

Whole body and hematopoietic ADAM8 deficiency does not influence advanced atherosclerotic lesion development, despite its association with human plaque progression

C. Weber, T. Theelen, A. Ludwig, 2017, Scientific Reports.

Differentiation factors and cytokines in the atherosclerotic plaque micro-environment as a trigger for macrophage polarisation

M. D. de Winther, M. Donners, Ine M. J. Wolfs, 2011, Thrombosis and Haemostasis.

A Disintegrin and Metalloprotease 10 Is a Novel Mediator of Vascular Endothelial Growth Factor–Induced Endothelial Cell Function in Angiogenesis and Is Associated With Atherosclerosis

J. Waltenberger, D. Molin, J. V. van Buul, 2010, Arteriosclerosis, thrombosis, and vascular biology.

Deleting myeloid IL-10 receptor signalling attenuates atherosclerosis in LDLR-/- mice by altering intestinal cholesterol fluxes

L. Beckers, Werner Müller, A. Groen, 2016, Thrombosis and Haemostasis.

Myeloid A disintegrin and metalloproteinase domain 10 deficiency modulates atherosclerotic plaque composition by shifting the balance from inflammation toward fibrosis.

L. Schurgers, S. Rose-John, P. Saftig, 2015, The American journal of pathology.

Hematopoietic miR155 Deficiency Enhances Atherosclerosis and Decreases Plaque Stability in Hyperlipidemic Mice

B. Schroen, S. Heymans, M. Gijbels, 2012, PloS one.

Reprogramming macrophages to an anti‐inflammatory phenotype by helminth antigens reduces murine atherosclerosis

L. Beckers, M. Gijbels, E. Biessen, 2014, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

Hck/Fgr Kinase Deficiency Reduces Plaque Growth and Stability by Blunting Monocyte Recruitment and Intraplaque Motility

V. Hérias, R. Koenen, C. Weber, 2015, Circulation.

Whole body and hematopoietic ADAM8 deficiency does not influence advanced atherosclerotic lesion development, despite its association with human plaque progression

C. Weber, T. Theelen, A. Ludwig, 2017, Scientific Reports.