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CD56 + CD8+ T cells straddle innate and adaptive immunity, distinguished by natural killer receptor (NKR) expression and the capacity for TCR-independent, bystander effector functions. These cells are implicated in liver inflammation and may represent a barrier to immune restoration in chronic hepatitis B (CHB). Given emerging evidence that metabolic dysfunction-associated steatotic liver disease (MASLD) co-existing with CHB (CHB-MASLD) is associated with delayed viral responses and persistent inflammation, understanding the behaviour of CD56+ CD8+ T cells may provide insights into immunometabolic dysregulation relevant to both CHB and CHB-MASLD.We investigated circulating CD8+ T cells in healthy controls (HC) and CHB patients (treatment-naïve and on antiviral therapy, AVT). Multi-parameter flow cytometry was used to assess activation status, NKR expression, response to free fatty acids (FFAs), and effector function. CD8+ T cells were also sorted for transcriptomic analysis.Activated (CD38+HLA-DR+) CD8+ T cells expressing CD56 were significantly expanded in CHB patients compared to HCs, with increased expression of NKRs (NKG2A, NKp30). These innate-like CD56+ CD8+ T cells were more prevalent in ‘immune active’ than ‘immune control’ disease. AVT-treated patients had reduced proportions of CD56+ CD8+ T cells, yet their NKR expression remained high, indicating persistent innate-like signatures. Transcriptomic profiling revealed upregulation of innate-associated genes (e.g., KLRK1, NCR3) in AVT-treated patients compared to untreated controls. Functionally, CD56+ CD8+ T cells showed comparable IFN-γ production following TCR-dependent (anti-CD3/CD28) and TCR-independent (IL-15) stimulation, but TNF-α production was significantly higher following IL-15 stimulation, confirming a differential functional and bystander activation profile. These cells were also more susceptible to suppression by FFAs, suggesting functional vulnerability in metabolically altered environments.Our findings show that CD56+ CD8+ T cells with innate-like features are expanded and functionally distinct in CHB, with persistent NKR expression despite AVT and heightened sensitivity to metabolic cues. The susceptibility of these cells to FFAs supports a potential mechanistic link between metabolic dysfunction and immune dysregulation in CHB-MASLD. The exploration of the immunometabolic contribution of CD56+ CD8+ T cells to therapeutic resistance and liver disease progression appears critical in CHB and CHB-MASLD .