Interferon gamma (IFNγ) plays several roles in immune system regulation, inflammation and tumor surveillance. However, recent research led by Hussein Abbas, M.D., Ph.D., found that patients with newly diagnosed acute myeloid leukemia (AML) have elevated levels of IFNγ, leading to an immunosuppressed bone marrow microenvironment.
In a new study from the Abbas laboratory, researchers sought to characterize the role of IFNγ in the AML microenvironment. They discovered that T and NK cells are the main producers of IFNγ, suggesting that AML cells exploit this pathway to their advantage. IFNγ signaling strongly correlated with venetoclax treatment resistance in AML patient cells, and IFNγ treatment increased resistance to venetoclax therapy. Further, high IFNγ signaling was associated with poor clinical outcomes. The study uncovered new roles of IFNγ in AML immune biology, highlighting its potential as a therapeutic target.