The added value of type I interferons to cytotoxic treatments of cancer. (August 2017)

• Record Type: Journal Article
• Authors: Bracci, Laura; Sistigu, Antonella; Proietti, Enrico; Moschella, Federica
• Is Part Of: Cytokine & growth factor reviews. Volume 36(2017)
• Page Start: 89
• Page End: 97
• Publication Date: 2017-08
• Subjects: Ab antibody -- ATLL adult T-cell leukemia/lymphoma -- ATM ataxia-telangiectasia mutated -- Aza 5-azacytidine -- BAFF B-cell activating factor -- BM bone marrow -- cGAMP cyclic GMP-AMP -- cGAS cyclic GMP-AMP synthase -- CIC cancer initiating cell -- CRC colorectal cancer -- CSC cancer stem cell -- CTLA-4 cytotoxic T-lymphocyte antigen-4 -- CTX cyclophosphamide -- CXCL10 C-X-C motif chemokine ligand 10 -- Dac 5-aza-2-deoxycytidine -- DAMPs damage-associated molecular patterns -- DAI Z-DNA binding protein or ZBP-1 -- DC dendritic cell -- DDR DNA damage response -- DNMTi DNA methyltransferase inhibitor -- HER2 epidermal growth factor receptor 2 -- HMGB1 high mobility group box 1 -- HSPC hematopoietic stem/progenitor cell -- ICD immunogenic cell death -- IFI16 IFN-γ-inducible 16 -- IFITM interferon induced transmembrane protein -- IFNs interferons -- IFNAR1 IFN-α/β receptor 1 -- IL interleukin -- IRDS IFN-related DNA damage resistance signature -- ISG IFN stimulated gene -- ISGF3 IFN‐stimulated gene factor 3 -- JAK Janus kinase -- MAVS mitochondrial antiviral signalling adaptor -- MCA 3′-methylcholanthrene -- MDA5 melanoma differentiation-associated protein 5 -- miRNA microRNA -- MRE11 meiotic recombination 11 -- MyD88 myeloid differentiation primary response gene 88 -- Mx1 MX dynamin-like GTPase1 -- NF-κB nuclear factor–κB -- NK natural killer -- NLR NOD-like receptors -- NOTCH neurogenic locus notch homolog protein -- OAS 2' oligoadenylate synthetase -- OVA ovalbumin -- PBMC peripheral blood mononuclear cell -- PD-1 programmed-death-1 -- PD-L1 programmed death-ligand 1 -- PRR pattern recognition receptor -- RIG-I retinoic acid-inducible gene-I -- ROS reactive oxygen species -- RT radiotherapy -- SOCS suppressors of cytokine signalling -- STAT1 signal transducer and activator of transcription 1 -- STING stimulator of IFN genes -- TBK1 TANK-binding kinase 1 -- Th1 T helper 1 -- TLR Toll-like receptor -- TNF tumor necrosis factor -- TRIF TIR-domain containing adaptor protein-inducing IFN-β -- USP18 ubiquitin-specific peptidase 18 -- U-STAT1 unphosphorilated STAT1; Type I interferon -- Chemotherapy -- Radiotherapy -- Immunogenicity; Cytokines -- Periodicals; 571.84
• DOI: 10.1016/j.cytogfr.2017.06.008
• Languages: English
• ISSNs: 1359-6101

Abstract

Highlights: The therapeutic efficacy of some cytotoxic anticancer therapies relies on the induction of type I interferons in malignant or immune cells. Type I interferons released by dying tumor and/or tumor infiltrating immune cells enhances the immunogenicity of tumor associated antigens. Exogenous type I IFN administration can restore the immunogenicity of cell death following non-immunogenic treatments. Dying tumor cells along with type I interferons mimic an endogenous anti-tumor vaccination. Abstract: Type I interferons (IFNs) exert anti-proliferative, antiviral and immunomodulatory activities. They are also involved in cell differentiation and anti-tumor defense processes. A growing body of literature indicates that the success of conventional chemotherapeutics, epigenetic drugs, targeted anticancer agents and radiotherapy (RT) relies, at least in part, on the induction of type I IFN signaling in malignant cells, tumor-infiltrating antigen presenting cells or other immune cells within lymphoid organs or blood. The mechanisms underlying type I IFN induction and the clinical consequences of these observations are only beginning to be elucidated. In the present manuscript, we reviewed the recent advances in the field and provided our personal view on the role of type I IFNs induced in the context of cytotoxic anticancer treatments and on its possible exploitation as a complement in cancer therapy.