Chemokines in atherosclerotic lesion development and stability : from mice to man Jager, S.C.A. de

Peripheral blood cells were stained with HLA-A2.1 tetramers containing the tyrosinase368–376 peptide followed by staining with a panel of lineage antibodies, as described in

Representative MoMa-2 slides for controls (centre panel) and GRK2 +/- chimeras (right panel), macrophages are depicted in blue. Images 50x magniication. A) Collagen deposition

In the adventitia of the brachiocephalic artery BCA lesions, the percentage of activated mast cells at 7 days after mast cell activation was 62 ± 9% in controls, 75 ± 7% in

Figure 1: Induction of chronic Graft versus Host Disease in CCR7 -/- chimeras.A) Total number of bone marrow cells from WT controls (black) and CCR7 -/- chimeras (white).

Taken together our data clearly establish a causal role for neutrophils in the development of atherosclerosis Furthermore we hypothesize that under conditions of

Voor deze studie gebruikten wij een beenmergtransplantatiestrategie, waardoor de leukocyten in de bloedsomloop niet meer in staat zijn MIC-1 te produceren.. De afwezigheid van

Systemic mast cell activation induces atherosclerotic plaque progression in ApoE-/- miceS. Plasma chemokine proiling of myocardial infarction patients by a luorescence

Mestcelactivatie resulteert niet alleen in een versnelde progressie van atherosclerose maar bevordert tevens de vorming van ruptuur-gevoelige plaques (ditproefschrift,