Hepatitis B immunoglobulin inhibits the secretion of HBV via antigen-antibody precipitation in the multivesicular body.

Background And Aims: Although the main action of human hepatitis B immunoglobulin (HBIG) is to neutralize hepatitis B virus surface antigen (HBsAg) in serum, HBIG is known to be localized in the cell. However, the effect of intracellularly located HBIG is poorly understood because of the low purity of conventional plasma-derived HBIG (cHBIG). We attempted to elucidate the mechanism of action of internalized HBIG using recombinant HBIG (lenvervimab).

Therapeutic Extracellular Vesicles from Tonsil-Derived Mesenchymal Stem Cells for the Treatment of Retinal Degenerative Disease.

Background: Retinal degenerative disease (RDD), one of the most common causes of blindness, is predominantly caused by the gradual death of retinal pigment epithelial cells (RPEs) and photoreceptors due to various causes. Cell-based therapies, such as stem cell implantation, have been developed for the treatment of RDD, but potential risks, including teratogenicity and immune reactions, have hampered their clinical application. Stem cell-derived extracellular vesicles (EVs) have recently emerged as a cell-free alternative therapeutic strategy; however, additional invasiveness and low yield of the stem cell extraction process is problematic.

Sirolimus Attenuates Calcineurin Inhibitor-Induced Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma.

Background: Calcineurin inhibitors (CNIs), which are potent immunosuppressants (ISs), increase the risk for hepatocellular carcinoma (HCC) recurrence after liver transplantation (LTx). Epithelial-mesenchymal transition (EMT) is a key process in which epithelial cancer cells lose their polarity, resulting in cancer progression and metastasis. The aim of this study was to evaluate the effect of sirolimus (SRL) individually and in combination with other ISs to reduce EMT.

Sirolimus and MMF are insufficient immunosuppressants for regulation of the proliferation of CD133+EpCAM+ cell populations in HCC cell lines.

Studies on effective immunosuppressive strategies for the management of patients undergoing a liver transplantation (LT) due to hepatocellular carcinoma (HCC) are limited. In the present study, immunosuppressive candidates predicted to exhibit beneficial immunosuppressive and tumor-suppressive effects in patients with HCC were assessed using Huh7 and HEP3B HCC cells, which have high proportions of CD133+EpCAM+ cancer stem cell (CSC) populations. The immunosuppressants assessed were sirolimus, tacrolimus, cyclosporine A and mycophenolate mofetil (MMF), and their activities were assessed on CSCs.

Impact of PNPLA3 (rs738409-G) polymorphism on post-transplant outcomes after liver transplantation for alcohol-related liver disease.

Introduction: We aimed to evaluate the association between PNPLA3 polymorphism and post-liver transplantation (LT) outcomes related to alcohol relapse (AR).

Method: We retrospectively analyzed data from patients receiving LT for alcoholic liver disease (ALD) from 04/2014 to 12/2017. Liver-related clinical outcomes were assessed by the gamma-glutamyltransferase (GGT) level and alcohol-related liver failure (ARLF).

Sirolimus and Metformin Synergistically Inhibits Colon Cancer In Vitro and In Vivo.

We estimated the effect of various immunosuppressants (ISs) and metformin (M) to provide theoretical background of optimal therapeutic strategy for de novo colon cancer after liver transplantation (LT). Three colon cancer cell lines (HT29, SW620, and HCT116) were used in in vitro studies. HT29 was also used in BALB/c-nude mice animal models.

Effect of PNPLA3 I148M polymorphism on histologically proven non-alcoholic fatty liver disease in liver transplant recipients.

Aim: PNPLA3 I148M polymorphism (rs738409 C>G) is the most important and best-known polymorphism for non-alcoholic fatty liver disease (NAFLD). However, little is known about the effect of this polymorphism on NAFLD after liver transplantation (LT). We aimed to evaluate the association between this polymorphism and post-LT NAFLD.