Impact of Hypothermic Perfusion on Immune Responses and Sterile Inflammation in a Preclinical Model of Pancreatic Transplantation.

Background: In organ transplantation, cold ischemia is associated with sterile inflammation that subsequently conditions adaptive immunity directed against the grafts during revascularization. This inflammation is responsible for venous thrombosis, which is the main postoperative complication affecting graft function. Our aim was to investigate the modulation of immune responses and endothelial function of pancreatic grafts during cold ischemia using different preservation modalities.

Characterization of binding sites for neuropeptide FF on T lymphocytes of the Jurkat cell line.

Neuropeptide FF (NPFF) is a neuropeptide with antiopiate properties able to antagonize the action of both endogenous and exogenous opiates. Because we have recently shown that NPFF modulates the proliferation of human T lymphocytes, we have searched for binding sites for this peptide on T lymphocytes. Our study shows that T lymphocytes of the Jurkat cell line express binding sites for [125I]YLFQPQRFamide, an iodinated analogue of NPFF.

Modulation of human lymphocyte proliferation by FLFQPQRFamide, a FMRFamide-like peptide with anti-opiate properties.

The octapeptide Phe-Leu-Phe-Gln-Pro-Gln-Arg-Phe-NH2 (F8Fa), originally detected in mammalian brain by antisera raised against the invertebrate peptide Phe-Met-Arg-Phe-NH2 (FMRFamide) is a neuropeptide able to antagonize the actions of both endogenous and exogenous opiates. Since it is well accepted that lymphocytes are targets for opiates, we have tested the effect of F8Fa on T cell proliferation from normal human peripheral blood lymphocytes. Our study shows that F8Fa exerts a concentration-dependent diphasic modulation of human T lymphocyte proliferation.