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96 reviewsChronic hepatitis B virus (HBV) infection is marked by dysfunctional HBV-specifc CD8+ T cells, and restoring their efector activity is a major therapeutic goal. Here, we generated HBV-specifc CD4+ T cell receptor transgenic mice to show that CD4+ efector T cells can prevent and reverse the CD8⁺ T cell dysfunction induced by hepatocellular priming. This rescue enhances antiviral CD8+ T cell function and suppresses viral replication. CD4+ T cell help occurs directly within the liver, independent of secondary lymphoid organs, and requires local antigen recognition. Kupfer cells, rather than dendritic cells, are the critical antigen-presenting platform. CD4+ T cells license Kupfer cells via CD40–CD40L interactions, triggering interleukin (IL)-12 and IL-27 production. IL-12 expands the CD4+ T cell pool, while IL-27 is essential for CD8+ T cell rescue. Exogenous IL-27 similarly restores HBV-specifc CD8+ T cell function in mice and in T cells isolated from chronically infected patients. These fndings identify IL-27 as a tractable immunotherapeutic target in chronic HBV infection.
