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Hepatitis B virus (HBV)-specific CD4+ and CD8+ T cells are essential for the immune-mediated clearance of HBV-infected cells. In chronic hepatitis B, these T cells often enter a state of exhaustion or are deleted, preventing the host from achieving a functional cure (Maini & Pallett, 2018). The therapeutic approach of activating these cells via antigen-presenting dendritic cells (DCs) involves the uptake, processing, and presentation of HBV antigens (such as HBsAg or HBcAg) by DCs to T cells. This interaction, occurring via MHC-TCR binding and co-stimulation, aims to re-prime and expand the HBV-specific T-cell repertoire (Bertoletti & Ferrari, 2012). Activated CD8+ T cells then target infected hepatocytes for destruction or non-cytolytic viral suppression, while CD4+ T cells provide critical help for maintaining the immune response. This strategy is currently being explored through various therapeutic vaccines and ex vivo cell therapies designed to overcome the immune tolerance characteristic of chronic HBV infection (Gehring & Protzer, 2019).
Activation and expansion of HBV-specific T cells through the presentation of viral antigens by dendritic cells, leading to the destruction of infected hepatocytes and suppression of viral replication (Bertoletti & Ferrari, 2012; Gehring & Protzer, 2019).
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