作者: Marie-C??cile Michallet , Xavier Preville , Monique Flacher , Sylvie Fournel , Laurent Genestier
DOI: 10.1097/01.TP.0000053198.99206.E6
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摘要: BACKGROUND Polyclonal antithymocyte globulins (ATG) induce T-cell depletion and functional impairment of nondeleted lymphocytes. Interference ATG with the main leukocyte surface molecules involved in cellular adhesion leukocyte-endothelium interaction was investigated present study. METHODS In three rabbit ATG, authors measured antibodies to integrins, beta2-integrin ligands, chemokine receptors by flow cytometry; chemotactic responses; down-modulation cell expression on lymphocytes, monocytes, neutrophils. RESULTS Antibodies CD11a/CD18 (leukocyte function-associated antigen-1 [LFA-1]) induced a dose-dependent this beta2 integrin contrast, anti-LFA-1 monoclonal did not LFA-1 modulation unless cross-linked second antibody. also contained beta1 CD49d/CD29 (VLA-4), alpha4beta7 integrin, CD50, CD54, CD102 but CD62L. were shown bind CXCR4 CCR7 CXCR4, CCR5 monocytes; down-modulate CCR7; decrease monocyte response CCL5 (RANTES) lymphocyte CCL19 (MIP-3beta). CONCLUSION These results show that may interfere responses signals mostly inhibit integrins required for firm adhesion. The latter property inhibition is shared antibodies, it contribute decreasing graft infiltration during acute rejection possibly after postischemic reperfusion.