[[Macrophage]]-mediated [[tumor]] [[cell]] [[phagocytosis]] and subsequent [[neoantigen]] presentation are critical for generating anti-tumor [[immunity]]. A study aimed to uncover the potential clinical value and molecular mechanisms of MicroRNA-22 (miR-22) in tumor cell phagocytosis via macrophages and more efficient [[T cell]] priming. Tu et al. found that miR-22 expression was markedly downregulated in primary macrophages from [[glioma]] tissue samples compared to adjacent tissues. miR-22-overexpressing macrophages inhibited [[glioma]] cell [[proliferation]] and [[migration]], respectively. miR-22 upregulation stimulated the phagocytic ability of macrophages, enhanced tumor cell phagocytosis, antigen presentation, and efficient T cell priming. Additionally, our data revealed that miR-22-overexpressing macrophages inhibited glioma formation in vivo, HDAC6 was a target, and NF-κB signaling was a pathway closely associated with miR-22 in tumor-associated macrophages (TAMs) of glioma. Our findings revealed the essential roles of miR-22 in tumor cell phagocytosis by macrophages and more efficient T cell priming, facilitating further research on phagocytic regulation to enhance the response to tumor immunotherapy
((Tu J, Fang Y, Han D, Tan X, Xu Z, Jiang H, Wang X, Hong W, Wei W. MicroRNA-22 represses glioma development via activation of macrophage-mediated innate and adaptive immune responses. Oncogene. 2022 Mar 12. doi: 10.1038/s41388-022-02236-7. Epub ahead of print. PMID: 35279703.))