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Macrophages are involved in tumor growth and progression. They infiltrate into tumors and cause inflammation, which creates a microenvironment favoring tumor growth and metastasis. However, certain stimuli may induce macrophages to act as tumor terminators. Here we report that the calcineurin B subunit (CnB) synergizes with IFN- γ  to make macrophages highly cytotoxic to cancer cells. Furthermore, CnB and IFN- γ  act synergistically to polarize mouse tumor-associated macrophages, as well as human monocyte-derived macrophages to an M1-like phenotype. This synergy is mediated by the crosstalk between CnB-engaged integrin  α M-p38 MAPK signaling and IFN- γ -initiated p38/PKC- δ /Jak2 signaling. Interestingly, the signal transducer and activator of transcription 1 (STAT1) is a key factor that orchestrates the synergy of CnB and IFN- γ , and the phosphorylation status at Ser727 and Tyr701 of STAT1 is directly regulated by CnB and IFN- γ .

The synergistic interaction between the calcineurin B subunit and IFN-γ enhances macrophage antitumor activity