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Stefania Crotta

Researcher at Francis Crick Institute

Publications -  42
Citations -  3295

Stefania Crotta is an academic researcher from Francis Crick Institute. The author has contributed to research in topics: Virus & Influenza A virus. The author has an hindex of 22, co-authored 39 publications receiving 2488 citations. Previous affiliations of Stefania Crotta include University of Milan & John Radcliffe Hospital.

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Inhibition of Natural Killer Cells through Engagement of CD81 by the Major Hepatitis C Virus Envelope Protein

TL;DR: It is reported that ligation of an HCV receptor (CD81) inhibits natural killer (NK) cells, implicate HCV-E2–mediated inhibition of NK cells as an efficient HCV evasion strategy targeting the early antiviral activities ofNK cells and allowing the virus to establish itself as a chronic infection.
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Pathogenic potential of interferon αβ in acute influenza infection

TL;DR: Excessive IFNαβ signalling in response to acute influenza infection can result in uncontrolled inflammation and TRAIL-DR5-mediated epithelial cell death, which may explain morbidity and has important implications for treatment of severe disease.
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Type I and III interferons disrupt lung epithelial repair during recovery from viral infection.

TL;DR: It is shown that IFN signaling interferes with lung repair during influenza recovery in mice, with IFN-λ driving these effects most potently, and the location, timing, and duration of IFN exposure are critical parameters underlying the success or failure of therapeutics for viral respiratory infections.
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Type I and Type III Interferons Drive Redundant Amplification Loops to Induce a Transcriptional Signature in Influenza-Infected Airway Epithelia

TL;DR: It is shown that airway epithelia, the primary target of influenza A virus, produce both IFN I and III upon infection, and that induction of both depends on the RIG-I/MAVS pathway.
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The Environmental Sensor AHR Protects from Inflammatory Damage by Maintaining Intestinal Stem Cell Homeostasis and Barrier Integrity

TL;DR: Deletion of Ahr in intestinal epithelial cells results in a defective barrier and unrestricted proliferation of intestinal stem cells (ISCs), culminating in malignant transformation, and activation of AHR by dietary ligands guards the ISC niche and maintains intestinal barrier homeostasis.