Type I interferons in anticancer immunity
By L. Zitvogel, L. Galluzzi, Oliver Kepp, M. Smyth, Guido Kroemer. Nature reviews. Immunology, 2015
1,152 citations recorded by the source corpus.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/5c57f91e9b2c3547319eb3f5d85409cba53c53ad
How researchers see this paper
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In Immunology
- Guido Kroemer
- L. Galluzzi
- L. Zitvogel
- Simone Fulda
- Junying Yuan
- Oliver Kepp
- Douglas R. Green
- K. Debatin
Citations in the corpus
- Impact of microbiota on central nervous system and neurological diseases: the gut-brain axis (2019, background): “IFN-I has also been shown to stimulate the maturation of DC and enhancement of cytotoxic T cells, which are crucial for immune responses against cancers [31].”
- Autophagy in inflammation, infection, and immunometabolism (2021, background): “Thus, given that type I IFN plays an important anti-cancer role in general (Zitvogel et al., 2015), and that cGAS synergizes with immune check point blockade by anti-PDL-1 antibody (Wang et al.”
- Clinical significance of tumor-infiltrating lymphocytes in breast cancer (2016, background): “CD8 cytotoxic T-cells (CTL) are essential for tumor destruction [6].”
- Immunological Effects of Conventional Chemotherapy and Targeted Anticancer Agents. (2015, background): “As a notable example, type I interferon (IFN) not only plays a cardinal role in the control of viral spreading but also is essential for the immunological control of cancer cells (Zitvogel et al., 2015).”
- Necroptosis: Mechanisms and Relevance to Disease (2016, neutral): “ZBP1 responds to exogenous DNA in the cytosol by promoting the synthesis of type I interferon (IFN) and downstream components of type I IFN responses (96, 97), as well as by activating NF-κ B signaling (93, 98).”
- Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “Further underscoring the complexity of the interaction between inflammation and pyroptosis [649], CASP11 can also be upregulated by a complement cascade dependent on carboxypeptidase B1 (CPB1) acting downstream of TLR4 and IFNAR1 activation [650].”