Background/Objectives: Immune checkpoint inhibitors (ICIs) have become part of standard systemic therapy for hepatocellular carcinoma (HCC), yet only a minority of patients achieve durable responses. The immunosuppressive tumour microenvironment (TME) is increasingly recognised as a central determinant of this resistance, but existing literature largely treats individual TME components – tumour-associated macrophages, neutrophils, myeloid-derived suppressor cells, regulatory T cells, cancer-associated fibroblasts, exhausted T cells and others – as independent contributors. This review aimed to synthesise current cellular, molecular and spatial evidence on the HCC TME into a unified, systems-level explanation of ICI resistance. Methods: A literature search was conducted in PubMed/MEDLINE, Scopus and Web of Science Core Collection, combining terms for HCC, the TME, individual TME cell populations, and methodological/therapeutic aspects, supplemented by a snowballing search of reference lists and a direct search of ClinicalTrials.gov for relevant trials. Results: The review characterises the physiological basis of hepatic immune tolerance and its pathological co-option in HCC, the principal immunosuppressive cell populations and their intercellular network, the contribution of the gut and intratumoural microbiome, and the spatial architecture of the TME, including the invasive tumour margin. Integrating these findings, we propose five interrelated principles of TME-centred ecosystem resistance – immune exclusion, distributed robustness, functional entrapment, multiscale feedback stabilisation, and surface–depth mismatch – that jointly explain why single-checkpoint blockade is frequently insufficient. Conclusions: Overcoming ICI resistance in HCC requires combination strategies that target multiple, interacting nodes of the suppressive TME network rather than the PD-1/PD-L1 axis alone, guided by aetiology-aware, spatially resolved biomarkers.