Type I Interferons: A Double-Edged Sword of Immune Regulation and Cancer Progression

Dear Colleagues,

Interferons (IFNs) are a family of pleiotropic cytokines, which play a key role in a wide range of biological processes. In addition to the well-described antiviral actions, IFNs were quickly recognized as central coordinators of innate immune responses during tumorigenesis. However, evidence has emerged in recent years suggesting that IFNs may also trigger immune suppressive mechanisms in cancer-promoting malignant progression and resistance to therapies. Depending on the stimulus, IFNs can be produced by almost any cell type, including fibroblasts and leucocytes, as well as cancer cells, through the engagement of distinct pattern recognition receptors (PRRs). In this regard, danger-associated molecular patterns (DAMPs) released upon cellular stress or therapy-induced cell death represent key inducers of type I IFNs in the tumor microenvironment. Among sensing pathways, a major role is played by the cGAS-STING pathway, which detects cytoplasmic DNA after DNA damage. A growing amount of evidence indicates that the cGAS-STING pathway has a role in regulating other important cellular processes such as autophagy, cell survival, and senescence.

For this Special Issue of Biology, we invite authors to submit original research papers, review articles, commentaries, and perspective pieces on recent progress in the broad topic of Type-I-IFNs in cancer diseases, including cancers transformed by an oncogenic virus (i.e., HPV, EBV), highlighting their dichotomous role and the potential therapeutic benefit of type I IFN pathway modulation.

Prof. Alessandra Soriani
Prof. Alessandra Zingoni
Guest Editors

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