Abstract
NEUTROPHIL-mediated inflammation is involved in a number of human clinical manifestations, including the adult respiratory distress syndrome, multi-organ failure and reperfusion injury1. One way of inhibiting this type of inflammatory response would be to block competitively the adhesive interactions between neutrophils and the endothelium adjacent to the inflamed region2. The lectin-containing3,4murine adhesion molecule gp90MEL, the homing receptor, is found on all leukocytic cells, including neutrophils5. MEL14, a monoclonal antibody directed against this adhesion molecule, blocks lymphocyte traffic to lymph nodes6 and extravasation of neutrophils from blood to inflammatory sites7. Here we show that administration to mice of a soluble immunoglobulin chimaera containing the murine homing receptor extracellular domain significantly decreases the number of neutrophils that migrate to the peritoneum in response to the inflammatory irritant thioglycollate. These results indicate that soluble forms of a single type of adhesion molecule, the homing receptor, could be clinically effective compounds for the inhibition of neutrophil-mediated inflammation.
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Watson, S., Fennie, C. & Lasky, L. Neutrophil influx into an inflammatory site inhibited by a soluble homing receptor–IgG chimaera. Nature 349, 164–167 (1991). https://doi.org/10.1038/349164a0
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DOI: https://doi.org/10.1038/349164a0
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