Mitochondrial checkpoint for interferon responses in macrophages
Andreas O. Mieland , Oliver H. Krämer
Exploration of Targeted Anti-tumor Therapy ›› 2026, Vol. 7 ›› Issue (1) : 1002399
A functional immune system is a key antagonist of cancer cell growth. Cytokines such as interferons (IFNs) promote the onset of inflammation, turn cells into an anti-viral state, and shape the dynamic tumor-immune cell interactome. Recent work illustrates how type I IFNs contribute to the resolution of inflammatory conditions. This involves macrophage-mediated efferocytosis for the clearance of apoptotic cells and the intrinsic capacity of type I IFNs to restrict their own autocrine signaling loops via the IFN-stimulated gene 15 (ISG15) protein. We discuss how this may affect tumor cells and how acetylation-dependent processes can affect the phosphorylation-dependent signaling cascades that augment IFN-dependent gene expression.
acetylation / efferocytosis / histone deacetylase (HDAC) / JAK-STAT / gene expression / interferon / ISG15 / macrophage
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