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Ed and sections were stained. (A) Photomicrographs of staining for VWF

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Ed and sections were stained. (A) Photomicrographs of staining for VWF after 1 h. (B) Quantitation or VWF release after 1 h (n 8 SD; *, P 0.04). (C) Photomicrographs of staining for MPO in dermal vessels after 1 h. Clusters of cells in small vessels stain for MPO in antibody-treated grafts. (D) Quantitation of MPO-positive cells after 1 h (n 8 SD; *, P 0.03). (E) Quantitation of VWF release after
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To HLA activates endothelial exocytosis, releasing VWF and externalizing P-selectin, which

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To HLA activates endothelial exocytosis, releasing VWF and externalizing P-selectin, which lead to platelet aggregation and leukocyte infiltration. Discussion The major finding of this study is that antibody to HLA activates endothelial exocytosis in vitro and in vivo. These data suggest that one mechanism for antibody injury to transplanted organs is through antibody-triggering endothelial cell e
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S with equivalent event selections which had been performed with information collected

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Tibody activation of exocytosis depends upon cross-linking HLA class I, because

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Tibody activation of exocytosis depends upon cross-linking HLA class I, because an individual Fab fragment could not activate exocytosis (Fig. 5A). Furthermore, cross-linking the monovalent Fab restored antibody induced exocytosis (Fig. 5B). How is cross-linking of HLA class I coupled to the exocytic machinery? Prior studies have shown that antibodies to HLA canYamakuchi et al.Fig. 7. Antibody to
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