Effect of protein C gene mutation on coagulation and inflammation in hemorrhagic shock.

Introduction: Trauma patients are at high risk of complications and death from coagulopathy and inflammatory organ failure. Recent evidence implicates protein C (PC) as a key mediator of this process. We hypothesized that a mutation in the PC gene would ameliorate the inflammatory and coagulopathic response to hemorrhagic shock (HS) and resuscitation.

Soluble donor-like MHC class I proteins induce CD4(+)CD25(+)CD8(-)FoxP3(+) cells with potential to ameliorate graft chronic injury.

Conventional immunosuppressive therapies failed to prevent allograft chronic rejection. New approaches to modulate recipient immune response are needed. Donor-like MHC class I soluble proteins demonstrated therapeutic potential to suppress chronic rejection.

Intensity of transplant chronic rejection correlates with level of graft-infiltrating regulatory cells.

Background: The understanding of chronic rejection (transplant vascular sclerosis, or TVS) mechanisms is a major goal of transplantation. In this study we tested a cardiac transplant model for TVS development in connection with emerging T-regulatory cells (T-regs). We used 40-mer peptides derived from the donor MHC Class I alpha1 helix of the alpha1-domain to make recipients tolerant.