Abstract
This study has enabled us to identify the influence of the chemokine, macrophage inflammatory protein-1alpha (MIP-1alpha), on leukocyte behavior at the blood-retina barrier in vivo and its link with the inflammatory process and disease pathogenesis. MIP-1alpha has not previously been thought to be effective under conditions of physiological shear flow. However, short-term anti-MIP-1alpha 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-1alpha treatment also prevented decreased leukocyte velocity and reduced disease severity as measured clinically, histologically and in terms of blood-retina barrier breakdown.
Original language | English |
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Pages (from-to) | 402-410 |
Number of pages | 8 |
Journal | European Journal of Immunology |
Volume | 33 |
Issue number | 2 |
DOIs | |
Publication status | Published - Feb 2003 |
Keywords
- macrophage inflammatory protein-1 alpha
- CCL3
- chemokine
- cell trafficking
- inflammation
- ROLLING T-LYMPHOCYTES
- ENDOTHELIAL-CELLS
- FLOW CONDITIONS
- CUTTING EDGE
- CHEMOKINE
- ENCEPHALOMYELITIS
- UVEITIS
- ARREST
- MIP-1-ALPHA
- EXPRESSION