Enhancing HBV-specific T cell responses through a combination of epigenetic modulation and immune checkpoint inhibition.

Background And Aims: Chronic HBV infection exhausts HBV-specific T cells, develops epigenetic imprints that impair immune responses, and limits the effectiveness of immune checkpoint inhibitor monotherapy, such as anti-programmed cell death ligand-1 antibody (αPD-L1). This study aimed to determine whether the DNA methyltransferase inhibitor decitabine (DAC) could reverse these epigenetic imprints and enhance immune checkpoint inhibitor efficacy in restoring HBV-specific T cell responses.

Approach And Results: We investigated HBV-specific T cell responses by 10-day in vitro stimulation of peripheral blood mononuclear cells (PBMCs) from patients with chronic HBV infection.

Characterization of Endogenous SERINC5 Protein as Anti-HIV-1 Factor.

When expressed in virus-producing cells, the cellular multipass transmembrane protein SERINC5 reduces the infectivity of HIV-1 particles and is counteracted by HIV-1 Nef. Due to the unavailability of an antibody of sufficient specificity and sensitivity, investigation of SERINC5 protein expression and subcellular localization has been limited to heterologously expressed SERINC5. We generated, via CRISPR/Cas9-assisted gene editing, Jurkat T-cell clones expressing endogenous SERINC5 bearing an extracellularly exposed hemagglutinin (HA) epitope [Jurkat (iHA knock-in) T cells].