ArticleOncoimmunology2012
Conditional IFNAR1 ablation reveals distinct requirements of Type I IFN signaling for NK cell maturation and tumor surveillance.
Article in Oncoimmunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 67 citations in OpenAlex.
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- JAK inhibitor withdrawal causes a transient pro-inflammatory cascade: A potential mechanism for major adverse cardiac events.PloS one · 2025Article
- Iron Chelation Therapy Elicits Innate Immune Control of Metastatic Ovarian Cancer.Cancer discovery · 2024Article
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- Bystander activated CD8Nature communications · 2024Article
- Intrinsic suppression of type I interferon production underlies the therapeutic efficacy of IL-15-producing natural killer cells in B-cell acute lymphoblastic leukemia.Journal for immunotherapy of cancer · 2023Article
- The spectrum of sex differences in cancer.Trends in cancer · 2022Review
- Widespread discrepancy ineLife · 2022Article
- Consequences of sex differences in Type I IFN responses for the regulation of antiviral immunity.Frontiers in immunology · 2022Review
- Type I interferon subtypes differentially activate the anti-leukaemic function of natural killer cells.Frontiers in immunology · 2022Article
- Triple-negative breast cancer cells rely on kinase-independent functions of CDK8 to evade NK-cell-mediated tumor surveillance.Cell death & disease · 2021Article
- Review
- Loss of type I IFN responsiveness impairs natural killer cell antitumor activity in breast cancer.Cancer immunology, immunotherapy : CII · 2021Article
- Opioids drive breast cancer metastasis through the δ-opioid receptor and oncogenic STAT3.Neoplasia (New York, N.Y.) · 2021Article
- Opposing Roles of Type I Interferons in Cancer Immunity.Annual review of pathology · 2021Review
- MYC functions as a switch for natural killer cell-mediated immune surveillance of lymphoid malignancies.Nature communications · 2020Article
Corrections and comments
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Authors and funding
17 authors at 8 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mice with an impaired Type I interferon (IFN) signaling (IFNAR1- and IFNβ-deficient mice) display an increased susceptibility toward v-ABL-induced B-cell leukemia/lymphoma. The enhanced leukemogenesis in the absence of an intact Type I IFN signaling is caused by alterations within the tumor environment. Deletion of Ifnar1 in tumor cells (as obtained in Ifnar1(f/f) CD19-Cre mice) failed to impact on disease latency or type. In line with this observation, the initial transformation and proliferative capacity of tumor cells were unaltered irrespective of whether the cells expressed IFNAR1 or not. v-ABL-induced leukemogenesis is mainly subjected to natural killer (NK) cell-mediated tumor surveillance. Thus, we concentrated on NK cell functions in IFNAR1 deficient animals. Ifnar1(-/-) NK cells displayed maturation defects as well as an impaired cytolytic activity. When we deleted Ifnar1 selectively in mature NK cells (by crossing Ncr1-iCre mice to Ifnar1(f/f) animals), maturation was not altered. However, NK cells derived from Ifnar1(f/f) Ncr1-iCre mice showed a significant cytolytic defect in vitro against the hematopoietic cell lines YAC-1 and RMA-S, but not against the melanoma cell line B16F10. Interestingly, this defect was not related to an in vivo phenotype as v-ABL-induced leukemogenesis was unaltered in Ifnar1(f/f )Ncr1-iCre compared with Ifnar1(f/f) control mice. Moreover, the ability of Ifnar1(f/f) Ncr1-iCre NK cells to kill B16F10 melanoma cells was unaltered, both in vitro and in vivo. Our data reveal that despite the necessity for Type I IFN in NK cell maturation the expression of IFNAR1 on mature murine NK cells is not required for efficient tumor surveillance.
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Registered trials
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