Host type I IFN signals are required for antitumor CD8+ T cell responses through CD8α+ dendritic cells

By M. Fuertes, A. Kacha, J. Kline, Seng-Ryong Woo, D. Kranz, K. Murphy, T. Gajewski. Journal of Experimental Medicine, 2011

1,090 citations recorded by the source corpus.

The generation of antitumor CD8+ T cell responses requires type I interferon responsiveness in host antigen-presenting cells

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/acdca6eb672b69acb476f896b9b16d2430b3492d

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In Immunology

Citations in the corpus

The cGAS–cGAMP–STING pathway connects DNA damage to inflammation, senescence, and cancer (2018, background): “The activation of APCs requires type I IFN signaling initiated by innate immune sensors (Diamond et al., 2011; Fuertes et al., 2011).”
STING-Dependent Cytosolic DNA Sensing Mediates Innate Immune Recognition of Immunogenic Tumors (2014, background): “We therefore pursued a working model in which innate immune sensing pathways might detect tumor-derived factors, induce type I IFN production, and lead to cross-priming of tumor antigen-specific CD8+ T cells (Diamond et al., 2011; Fuertes et al., 2011).”
Tumor-residing Batf3 dendritic cells are required for effector T cell trafficking and adoptive T cell therapy (2017, methodology): “Significance was assumed with p % 0.05, with *p % 0.05, ***p % 0.001 ****p % 0.0001. to depend upon Batf3-driven DCs, and rejection of immunogenic tumors is ablated in Batf3 / mice (Broz et al., 2014; Edelson et al., 2010; Engelhardt et al., 2012; Fuertes et al., 2011; Roberts et al., 2016).”
Cyclooxygenase-Dependent Tumor Growth through Evasion of Immunity (2015, background): “DCs, especially the Batf3-dependent sub-family characterized by CD8a and/or CD103 expression, are essential for anti-cancer immune responses (Diamond et al., 2011; Fuertes et al., 2011; Hildner et al., 2008).”
Critical Role for CD103+/CD141+ Dendritic Cells Bearing CCR7 for Tumor Antigen Trafficking and Priming of T Cell Immunity in Melanoma (2016, neutral): “Based on the trafficking data in Figure 1, and observations of poor tumor control in Batf3 / animals lacking CD103+ and CD8a+ DC (Fuertes et al., 2011; Hildner et al., 2008), we hypothesized that the CD103+ DC were, in fact, the population of APC responsible for anti-tumor T cell priming.”
Structural design of engineered costimulation determines tumor rejection kinetics and persistence of CAR T cells (2015, neutral): “…delivery of IFNb as ‘‘Signal 3’’ could enhance tumor eradication inmultiple ways, by enhancing cross-priming activity of DCs (Diamond et al., 2011; Fuertes et al., 2011; Yang et al., 2014), inhibiting Treg activation and proliferation (Golding et al., 2010; Srivastava et al., 2014), and…”