Type I interferons in anticancer immunity

Zitvogel, Laurence; Galluzzi, Lorenzo; Kepp, Oliver; Smyth, Mark J.

doi:10.1038/nri3845

Cited by 1,055 publications

(945 citation statements)

References 127 publications

(114 reference statements)

Supporting

Mentioning

915

Contrasting

Unclassified

Order By: Relevance

“…62 Successful anticancer chemotherapeutic agents induce all these hallmarks of ICD, suggesting that they induce a sort of 'viral mimicry'. 37,63 From this point of view, the capacity of ICD inducers to trigger necroptosis-associated ICD would not consider an exception. By stimulating necroptosis, some widely used anticancer chemotherapeutics may restore anticancer immunosurveillance.…”

Section: Discussionmentioning

confidence: 99%

Contribution of RIP3 and MLKL to immunogenic cell death signaling in cancer chemotherapy

Yang¹,

Ma²,

Guo³

et al. 2016

OncoImmunology

Self Cite

155

145

View full text Add to dashboard Cite

Chemotherapy can reinstate anticancer immunosurveillance through inducing tumor immunogenic cell death (ICD). Here, we show that anthracyclines and oxaliplatin can trigger necroptosis in murine cancer cell lines expressing receptor-interacting serine-threonine kinase 3 (RIP3) and mixed lineage kinase domain-like (MLKL). Necroptotic cells featured biochemical hallmarks of ICD and stimulated anticancer immune responses in vivo. Chemotherapy normally killed Rip3 ¡/¡ and Mlkl ¡/¡ tumor cells and normally induced caspase-3 activation in such cells, yet was unable to reduce their growth in vivo. RIP3 or MLKL deficiency abolished the capacity of dying cancer cells to elicit an immune response. This could be attributed to reduced release of ATP and high mobility group box 1 (HMGB1) by RIP3 and MLKL-deficient cells. Measures designed to compensate for deficient ATP and HMGB1 signaling restored the chemotherapeutic response of Rip3 ¡/¡ and Mlkl ¡/¡ cancers. Altogether, these results suggest that RIP3 and MLKL can contribute to ICD signaling and tumor immunogenicity.

show abstract

Section: Discussionmentioning

confidence: 99%

Contribution of RIP3 and MLKL to immunogenic cell death signaling in cancer chemotherapy

Yang¹,

Ma²,

Guo³

et al. 2016

OncoImmunology

Self Cite

155

145

View full text Add to dashboard Cite

show abstract

“…3d). Type I IFNs have been shown to boost the effectiveness of the CD8+ T cell response 17,18 . We examined the expressions of IFN-stimulated genes (ISGs) in the local tissues 19 over time after subcutaneous injection of PC7A NP.…”

mentioning

confidence: 99%

“…3d–f), consistent with the ISG expression data. Toll-like receptors (TLR), MAVS and STING are known to activate the type I interferon pathways 17,21 . Immune response in MyD88 −/− /TRIF −/− , MAVS −/− or STING gt/gt mice showed that T cell response was not dependent on TLR or MAVS, whereas STING gt/gt mice almost recapitulated the phenotypes in IFN-α/βR −/− mice (Fig.…”

mentioning

confidence: 99%

A STING-activating nanovaccine for cancer immunotherapy

et al. 2017

View full text Add to dashboard Cite

Generation of tumor-specific T cells is critically important for cancer immunotherapy1,2. A major challenge in achieving a robust T cell response is the spatio-temporal orchestration of antigen cross-presentation in antigen presenting cells (APCs) with innate stimulation. Here we report a minimalist nanovaccine by a simple physical mixture of an antigen with a synthetic polymeric nanoparticle, PC7A NP, which generated a strong cytotoxic T cell response with low systemic cytokine expression. Mechanistically, PC7A NP achieved efficient cytosolic delivery of tumor antigens to APCs in draining lymph nodes leading to increased surface presentation while simultaneously activating type I interferon-stimulated genes. This effect was dependent on STING but not Toll-like receptor or MAVS pathway. Nanovaccine produced potent tumor growth inhibition in melanoma, colon cancer, and human papilloma virus-E6/E7 tumor models. Combination of PC7A nanovaccine with an anti-PD-1 antibody showed great synergy with 100% survival over 60 days in a TC-1 tumor model. Rechallenging of these tumor-free animals with TC-1 cells led to complete inhibition of tumor growth, suggesting generation of long-term antitumor memory. The STING-activating nanovaccine offers a simple, safe and robust strategy in boosting anti-tumor immunity for cancer immunotherapy.

show abstract

“…33 All three classes of IFNs, type I (IFN-a/b), type II (IFNg), and type three (IFN-λ/s), can induce apoptosis of tumor cells and control the circuits underlying cancer immunosurveillance. 34 IFNg promotes Th1 cell differentiation and classical macrophage M1 polarization. 13 Type I IFNs induce DC maturation, enhance cytotoxicity of CD8 C T and NK cells and decrease Treg immunosuppression.…”

Section: Cytokinesmentioning

confidence: 99%

The immune network in thyroid cancer

2016

View full text Add to dashboard Cite

The immune system plays critical roles in tumor prevention, but also in its initiation and progression. Tumors are subjected to immunosurveillance, but cancer cells generate an immunosuppressive microenvironment that favors their escape from immune-mediated elimination. During chronic inflammation, immune cells can contribute to the formation and progression of tumors by producing mitogenic, prosurvival, proangiogenic and lymphangiogenic factors. Thyroid cancer is the most frequent type of endocrine neoplasia and is the most rapidly increasing cancer in the US. In this review, we discuss recent findings on how different immune cells and mediators can contribute to thyroid cancer development and progression.

show abstract

Type I interferons in anticancer immunity

Cited by 1,055 publications

References 127 publications

Contribution of RIP3 and MLKL to immunogenic cell death signaling in cancer chemotherapy

Contribution of RIP3 and MLKL to immunogenic cell death signaling in cancer chemotherapy

A STING-activating nanovaccine for cancer immunotherapy

The immune network in thyroid cancer

Contact Info

Product

Resources

About