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

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Exploration of Targeted Anti-tumor Therapy ›› 2026, Vol. 7 ›› Issue (1) :1002399 DOI: 10.37349/etat.2026.1002399
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Mitochondrial checkpoint for interferon responses in macrophages
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Abstract

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.

Keywords

acetylation / efferocytosis / histone deacetylase (HDAC) / JAK-STAT / gene expression / interferon / ISG15 / macrophage

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Andreas O. Mieland, Oliver H. Krämer. Mitochondrial checkpoint for interferon responses in macrophages. Exploration of Targeted Anti-tumor Therapy, 2026, 7 (1) : 1002399 DOI:10.37349/etat.2026.1002399

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