Inflammation and immune responses are evoked locally by invasion and accumulation of immune cells into the lesion sites. The cell trafficking of immune cells into the tissue from the blood is closely regulated by a number of cell adhesion molecules and chemotactic factors including chemokines.
Fractalkine (FKN)/CX3CL1 is a membrane-bound chemokine possessing a chemokine/mucin hybrid structure and has a dual function as an adhesion molecule and a chemoattractant. FKN is mainly expressed on activated endothelial cells and its cognate receptor, CX3CR1, is expressed on cytotoxic effector lymphocytes and monocytes/macrophages. To date, a lot of important roles of the FKN-CX3CR1 axis has been identified: (1) the rapid capture and firm adhesion, (2) chemotaxis, (3) the enhancement of the transmigration, (4) the patrolling behavior of monocytes, (5) the accessory cell function and (6) the cell survival.
In this symposium, we will overview the pathological roles of the FKN-CX3CR1 axis in several inflammatory and autoimmune disease models revealed by anti-FKN mAb, and its distinct mode of action from other cytokine inhibitors.