In vivo analyses of early events in acute graft-versus-host disease reveal sequential infiltration of T-cell subsets.

Graft-versus-host disease (GVHD) is a major obstacle in allogeneic hematopoietic cell transplantation. Given the dynamic changes in immune cell subsets and tissue organization, which occur in GVHD, localization and timing of critical immunological events in vivo may reveal basic pathogenic mechanisms. To this end, we transplanted luciferase-labeled allogeneic splenocytes and monitored tissue distribution by in vivo bioluminescence imaging.

A truncated plasminogen activator inhibitor-1 protein blocks the availability of heparin-binding vascular endothelial growth factor A isoforms.

We have made deletions of the porcine plasminogen activator inhibitor-1 (PAI-1) gene to obtain recombinant truncated PAI-1 proteins to examine functions of the PAI-1 isoforms. We previously reported that one recombinant truncated protein, rPAI-1(23), induces the formation of angiostatin by cleaving plasmin. The rPAI-1(23) protein is also able to bind urokinase plasminogen activator and plasminogen and then reduce the amount of plasmin that is formed.