CD8(+) T 淋巴细胞在实体瘤中的浸润特征及调控机制：空间分布、生物学功能及其与免疫微环境的相互作用

CD8 + T lymphocytes are central effectors of anticancer immunity. Their abundance and spatial distribution within solid tumors are strongly correlated with patient prognosis and response to immune-checkpoint inhibitors (ICIs). Tumors have been categorized into "hot," "excluded," and "cold" types based on the infiltration patterns of CD8 + T cells, which reflect the underlying immune contexture and therapeutic potential.

However, many tumors remain resistant to T-cell infiltration, posing a significant barrier to immunotherapy. This review systematically outlines the seven critical steps of the Cancer-Immunity Cycle that govern CD8 + T-cell infiltration: antigen release, antigen processing and presentation, T-cell priming, trafficking through the vasculature, tumor infiltration, target recognition, and cytolytic activity.

At each step, tumor-intrinsic and microenvironmental barriers-including low tumor mutational burden, defective antigen-presenting machinery, immunosuppressive cytokines (e. g. , TGF-β, IL-10), abnormal vasculature, fibroblast-derived extracellular matrix, and inhibitory cell populations (e. g. , Tregs, MDSCs, TAMs)-can stall the immune response.

We further discuss the roles of immune-checkpoint signaling, metabolic competition, and suppressive cell networks in shaping T-cell exhaustion and exclusion.

Cutting-edge technologies-such as single-cell RNA-sequencing, spatial transcriptomics, imaging mass cytometry, and TCR repertoire profiling-have revealed spatial and functional heterogeneity within intratumoral CD8 + T cells and informed the design of rational combination therapies. Understanding and targeting these barriers is critical for converting immune-cold tumors into immune-infiltrated, therapy-responsive states.

We conclude with a perspective on the future of immunoengineering and immune-atlas integration to optimize CD8 + T-cell-based interventions in solid tumors.