Effect of anti‐macrophage inflammatory protein‐1α on leukocyte trafficking and disease progression in experimental autoimmune uveoretinitis

This study has enabled us to identify the influence of the chemokine, macrophage inflammatory protein‐1α (MIP‐1α), on leukocyte behavior at the blood‐retina barrier in vivo and its link with the inflammatory process and disease pathogenesis. MIP‐1α has not previously been thought to be effective under conditions of physiological shear flow. However, short‐term anti‐MIP‐1α treatment inhibited leukocyte slowing and accumulation and subsequent extravasation of leukocytes at the blood‐retina barrier in animals with experimental autoimmune uveoretinitis. This was effective predominantly in the post‐capillary venules which have been shown to be the main site of passage of leukocytes across the blood‐retina barrier. Long‐term anti‐MIP‐1α treatment also prevented decreased leukocyte velocity and reduced disease severity as measured clinically, histologically and in terms of blood‐retina barrier breakdown.