Title | Type I interferon and cancer. |
Publication Type | Journal Article |
Year of Publication | 2024 |
Authors | Holicek P, Guilbaud E, Klapp V, Truxova I, Spisek R, Galluzzi L, Fucikova J |
Journal | Immunol Rev |
Volume | 321 |
Issue | 1 |
Pagination | 115-127 |
Date Published | 2024 Jan |
ISSN | 1600-065X |
Keywords | Antineoplastic Agents, Cytokines, Humans, Interferon Type I, Neoplasms, Tumor Microenvironment |
Abstract | Type I interferon (IFN) is a class of proinflammatory cytokines with a dual role on malignant transformation, tumor progression, and response to therapy. On the one hand, robust, acute, and resolving type I IFN responses have been shown to mediate prominent anticancer effects, reflecting not only their direct cytostatic/cytotoxic activity on (at least some) malignant cells, but also their pronounced immunostimulatory functions. In line with this notion, type I IFN signaling has been implicated in the antineoplastic effects of various immunogenic therapeutics, including (but not limited to) immunogenic cell death (ICD)-inducing agents and immune checkpoint inhibitors (ICIs). On the other hand, weak, indolent, and non-resolving type I IFN responses have been demonstrated to support tumor progression and resistance to therapy, reflecting the ability of suboptimal type I IFN signaling to mediate cytoprotective activity, promote stemness, favor tolerance to chromosomal instability, and facilitate the establishment of an immunologically exhausted tumor microenvironment. Here, we review fundamental aspects of type I IFN signaling and their context-dependent impact on malignant transformation, tumor progression, and response to therapy. |
DOI | 10.1111/imr.13272 |
Alternate Journal | Immunol Rev |
PubMed ID | 37667466 |
Grant List | / / Leukemia and Lymphoma Society / CA271915 / / NIH/NCI / / / Sandra and Edward Meyer Cancer Center / / / Sotio Biotech / #I16-0064 / / STARR Cancer Consortium / / / US DoD BCRP / startup funds from the Dept. of Radiation Oncology / / Weill Cornell Medicine - Qatar / |