Hiroyasu Konno

TL;DR: An integrated RNA-sequencing approach demonstrates that CXCL13+ TH1-like cells are preferentially enriched in microsatellite-instable tumours from patients with colorectal cancer, and IGFLR1 is identified as a co-stimulatory molecule.

TL;DR: It is demonstrated here that, after autophagy-dependent STING delivery of TANK-binding kinase 1 to endosomal/lysosomal compartments and activation of transcription factors interferon regulatory factor 3 and NF-κB, STING is subsequently phosphorylated by serine/threonine UNC-51-like kinase (ULK1/ATG1), and IRF3 function is suppressed, thus preventing the persistent transcription of innate immune genes.

TL;DR: Impaired STING responses may enable damaged cells to evade host immunosurveillance processes, although they provide a critical prognostic measurement that could help predict the outcome of effective oncoviral therapy.

TL;DR: In this paper, the authors show that palmitoylation of STING at the Golgi is essential for activation of the interferon genes, and that 2-BP and Cys88/91Ser mutations are sufficient to prevent the activation of this pathway.

TL;DR: A role for STING is established in the control of cancer, significant insight is shed into the causes of inflammation-driven carcinogenesis and therapeutic strategies to help prevent malignant disease are shed.