Lentivirus-mediated PD-L1 overexpression in bone marrow-derived dendritic cells induces immune tolerance in a rat keratoplasty model.

Purpose: The side effects of immune suppressants on immune rejection have become increasingly apparent after keratoplasty. To find out new alternative immunotherapy strategies, we studied the role of programmed death-1 (PD-1) and its ligand (PD-L1) co-stimulatory pathway in inducing immune tolerance of rat keratoplasty.

Methods: The PD-L1 protein was constitutively overexpressed via lentiviral transduction in bone marrow-derived dendritic cells (BMDCs) from rats, then infused via the tail vein into rats before undergoing keratoplasty.

The role of soluble programmed death protein-1 (sPD-1) and soluble programmed death ligand-1 (sPD-L1) in rat corneal transplantation rejection.

Background: Immunological rejection is one of the problems in corneal transplantation. Recently, some research found out that soluble programmed death protein-1 (sPD-1) and soluble programmed death ligand protein-1 (sPD-L1) play a significant role in immunologic suppression.

Objectives: To explore expression of sPD-1 and sPD-L1 in a penetrative corneal transplantation model and its relationship with transplant rejection.

Protective effect of histatin 1 against ultraviolet-induced damage to human corneal epithelial cells.

The aim of the present study was to investigate the role of histatin 1 (Hst1) in human corneal epithelial cells (HCECs) exposed to ultraviolet (UV) radiation. Prior to UV irradiation for various durations, HCECs were pre-treated with different concentrations of Hst1 and the effect on cell apoptosis and cell viability were examined by flow cytometry, alamarBlue and MTT assays to determine the optimal concentration of Hst1 and UV dose. Cells were then subjected to quantitative PCR, ELISA and western blot analysis to determine the expression of cell damage-associated genes.

Inhibition of RelA expression via RNA interference induces immune tolerance in a rat keratoplasty model.

RelA, the most important regulator of NF-kB activity, and its mechanisms in keratoplasty immune rejection have not been fully investigated. In the present study, lentivirus-mediated silencing of RelA expression in a bone marrow-derived dendritic cell (BMDC) model was tested. The BMDCs were transfected with RelA-shRNA to induce an immature, maturation-resistant and tolerogenic phenotype, while not significantly changing IFN-γ, IL-10 and IL-17 expression.