In lieu of CML, xenoantibodies may facilitate endothelial cell changes by ADCC. NK cells, triggered by binding to the Fc region of anti-endothelial xenoantibodies, can disrupt them through perforin/granzyme-related mechanisms, or activate them by releasing TNFa. Furthermore, activated NK cells release interferon-y (IFNy) which can activate nearby monocytes and macrophages upregulating their expression of adhesion molecules and increasing their local accumulation. Through Fc- and Clq-receptors, monocytes and macrophages can also bind to anti-endothelial xenoantibodies. Subsequent activation leads to release of TNFa, NO, and reactive oxidant intermediates which can activate or injure endothelial cells; and proinflammatory cytokines, procoagulant factors, and complement components which may overwhelm local regulatory mechanisms.
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