Targeting IRG1 Reverses the Immunosuppressive Function of Tumor-Associated Macrophages and Enhances Cancer Immunotherapy

Mechanistically, tumor cells induced Irg1 expression in macrophages by activating NF-κB pathway, and itaconic acids produced by aconitate decarboxylase inhibited TET DNA dioxygenases to dampen the expression of inflammatory genes and the infiltration of CD8+ T cells into tumor sites.