Altered microRNA expression after infection with human cytomegalovirus leads to TIMP3 downregulation and increased shedding of metalloprotease substrates, including MICA.

Proteolytic shedding of ligands for the NK group 2D (NKG2D) receptor is a strategy used by tumors to modulate immune recognition by NK cells and cytotoxic T cells. A number of metalloproteases, especially those of the A disintegrin and metalloprotease (ADAM) family, can mediate NKG2D ligand cleavage and this process can be modulated by expression of the thiol isomerase ERp5. In this article, we describe that an increased shedding of the NKG2D ligand MICA is observed postinfection with several strains of human CMV due to an enhanced activity of ADAM17 (TNF-α converting enzyme) and matrix metalloprotease 14 caused by a reduction in the expression of the endogenous inhibitor of metalloproteases tissue inhibitors of metalloproteinase 3 (TIMP3).

Prostatic aspergillosis in a heart transplant recipient: case report and review.

In this study we report the first case of invasive prostatic aspergillosis (IPRA) in a heart recipient with post-transplantation antibody deficiency, and review the other 11 cases described in the medical literature. Seven patients were immunocompromised and 6 had dissemination to other sites. Examination of the prostate usually revealed enlargement, with or without nodular lesions.

Clostridium difficile-associated diarrhea in heart transplant recipients: is hypogammaglobulinemia the answer?

Background: Information regarding Clostridium difficile-associated diarrhea (CDAD) after solid-organ transplantation (SOT) is scarce, particularly after heart transplantation (HT). Although host immune response to C. difficile plays a substantial role in the outcome of this infection, the responsibility of hypogammaglobulinemia (HGG) as a predisposing condition for CDAD has not been studied in SOT.

Inhibition of brush border dipeptidase with cilastatin reduces toxic accumulation of cyclosporin A in kidney proximal tubule epithelial cells.

Background: Cilastatin reduces nephrotoxicity associated with cyclosporin A (CyA) in solid organ and bone marrow transplantation. This appears to be unrelated to changes in renal haemodynamics or CyA metabolism. How cilastatin induces this protection is unclear, but it could result from changes on accumulation of CyA proximal cells.