NEUTROPHIL INFLUX INTO AN INFLAMMATORY SITE INHIBITED BY A SOLUBLE HOMING RECEPTOR-IGG CHIMERA

NEUTROPHIL INFLUX INTO AN INFLAMMATORY SITE INHIBITED BY A SOLUBLE HOMING RECEPTOR-IGG CHIMERA
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DOI:
10.1038/349164a0
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发表时间:
1991-01-10
期刊:
影响因子:
64.8
通讯作者:
LASKY, LA
LASKY, LA
中科院分区:
综合性期刊1区
文献类型:
--
作者:
WATSON, SR;FENNIE, C;LASKY, LA

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Neutrophil-mediated inflammation is involved in a number of human clinical manifestations, including the adult respiratory distress syndrome, multi-organ failure and reperfusion injury 1. 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 region 2. The lectin-containing 3,4 murine adhesion molecule gp90MET, the homing receptor, is found on all leukocytic cells, including neutrophils. 5 MEL 14, a monoclonal antibody directed against this adhesion molecule, blocks lymphocyte traffic to lymph nodes 6 and extravasation of neutrophils from blood to inflammatory sites 7. 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.