Journal: Journal of Clinical Medicine

Article Title: Fractalkine Signalling (CX 3 CL1/CX 3 CR1 Axis) as an Emerging Target in Coronary Artery Disease

doi: 10.3390/jcm12144821

Figure Lengend Snippet: Role of fractalkine in leukocyte recruitment in vascular inflammation. Transmembrane chemokine CX 3 CL1 is expressed by inflamed vascular tissue, which then seizes CX 3 CR1-positive leukocytes from the circulation. Induced shedding of adhesion molecules would make it easier to separate bound leukocytes from the endothelium after the creation of cellular contact. This might cause the discharge of these cells back into the bloodstream or let leukocytes continue to move across and through the endothelium. Leukocytes would travel to the area of inflammation within the tissue by following a chemotactic gradient of soluble chemokines.

Article Snippet: These clinical associations have led to animal studies together with our collaborators at Kancera, which show in the rat MI model that CX 3 CR1 inhibition prior to reperfusion limits infarct size by 50%, and reduces neutrophil influx, oedema, and finally IMH (unpublished data [ ]).

Techniques:

Journal: Journal of Clinical Medicine

Article Title: Fractalkine Signalling (CX 3 CL1/CX 3 CR1 Axis) as an Emerging Target in Coronary Artery Disease

doi: 10.3390/jcm12144821

Figure Lengend Snippet: Mechanism of KAND567-mediated inhibition of the CX 3 CR1 receptor. KAND567 antagonises CX 3 CL1 binding and G-protein signalling by binding in an allosteric and non-competitive mode, intracellularly and close to the G-protein and beta-arrestin binding sites. As activating CX 3 CR1 triggers a cascade of multiple signalling pathways, one of the crucial pathways that KAND567 inhibits to provide its action is by inhibiting Ca 2+ mobilisation [ , ] and Src activation to activate focal adhesion kinase (FAK) and to prevent cellular migration [ , ].

Article Snippet: These clinical associations have led to animal studies together with our collaborators at Kancera, which show in the rat MI model that CX 3 CR1 inhibition prior to reperfusion limits infarct size by 50%, and reduces neutrophil influx, oedema, and finally IMH (unpublished data [ ]).

Techniques: Inhibition, Binding Assay, Activation Assay, Migration

Journal: Nephrology Dialysis Transplantation

Article Title: Distinct immunologic effects of different intravenous iron preparations on monocytes

doi: 10.1093/ndt/gft524

Figure Lengend Snippet: Expression of CCR5 and CX 3 CR1 as well as production of TNF-α, IL-1β and ROS in circulating mature classical, intermediate and nonclassical monocytes from control subjects

Article Snippet: The following antibodies were used: anti-CD14 PerCP (Mφ9), anti-CD16 PeCy7 (3G8) and anti-CD195 APC (2D7/CCR5) and anti-TNF FITC (MAb11) (BD Biosciences, Heidelberg, Germany), anti-CD86 PE (HA5.2B7) (Beckman-Coulter, Krefeld, Germany), anti-CX 3 CR1 FITC (2A9-1) (Biozol, Eching, Germany), and anti-IL-1β Alexa Fluor® 647 (JK1B-1) (Biolegend, Fell, Germany).

Techniques: Expressing, Control

Journal: Nephrology Dialysis Transplantation

Article Title: Distinct immunologic effects of different intravenous iron preparations on monocytes

doi: 10.1093/ndt/gft524

Figure Lengend Snippet: Expression of CCR5 and CX 3 CR1 and ROS production by in vitro differentiated classical and intermediate monocytes from control subjects

Article Snippet: The following antibodies were used: anti-CD14 PerCP (Mφ9), anti-CD16 PeCy7 (3G8) and anti-CD195 APC (2D7/CCR5) and anti-TNF FITC (MAb11) (BD Biosciences, Heidelberg, Germany), anti-CD86 PE (HA5.2B7) (Beckman-Coulter, Krefeld, Germany), anti-CX 3 CR1 FITC (2A9-1) (Biozol, Eching, Germany), and anti-IL-1β Alexa Fluor® 647 (JK1B-1) (Biolegend, Fell, Germany).

Techniques: Expressing, In Vitro, Control