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The gastric cancer tumor microenvironment is shaped by coordinated immune evasion, where tumor cells recruit suppressive populations (TAMs, MDSCs, and Tregs) and dampen effector T-cell and NK-cell function through checkpoint signaling, soluble mediators, and metabolic inhibitory circuits such as adenosine (155159) ( Supplementary Table 1 )

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Due to the continuous exposure to occlusal forces and periodontal microorganisms, alveolar bone possesses a unique immune microenvironment distinct from the long bones, with more frequent interactions between monocytes/macrophages and MSCs (Sima et al., 2019)