This suggests that H.pylori may recruit TAMs through specific pathways, with testable hypotheses including: (i) H.pylori drives Treg-mediated immunosuppression by recruiting CD163+ TAMs, verifiable via mIF assessing spatial co-localization between CCL19+ epithelial cells and CD163+ TAMs; (ii) CD86+ TAMs in CRC patients lose antigen-presenting capacity and undergo transformation into a ‘pseudo-activated’ state, testable through flow-sorted CD86+ TAMs co-cultured with CD8+ T cells followed by PD-1 expression analysis. The gene discussed is CD86; the disease is colorectal carcinoma.