Asset Details
Do you wish to reserve the book?
Interferon-λ and interleukin 22 act synergistically for the induction of interferon-stimulated genes and control of rotavirus infection
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Interferon-λ and interleukin 22 act synergistically for the induction of interferon-stimulated genes and control of rotavirus infection
Do you wish to request the book?
Interferon-λ and interleukin 22 act synergistically for the induction of interferon-stimulated genes and control of rotavirus infection
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Interferon-λ and interleukin 22 act synergistically for the induction of interferon-stimulated genes and control of rotavirus infection
2015
Overview
Epithelial surfaces are the main entry point for viruses and thus are important immunological sites. Diefenbach and colleagues show that the related cytokines IL-22 and IFN-λ act together in the control of enterovirus infection.
The epithelium is the main entry point for many viruses, but the processes that protect barrier surfaces against viral infections are incompletely understood. Here we identified interleukin 22 (IL-22) produced by innate lymphoid cell group 3 (ILC3) as an amplifier of signaling via interferon-λ (IFN-λ), a synergism needed to curtail the replication of rotavirus, the leading cause of childhood gastroenteritis. Cooperation between the receptor for IL-22 and the receptor for IFN-λ, both of which were 'preferentially' expressed by intestinal epithelial cells (IECs), was required for optimal activation of the transcription factor STAT1 and expression of interferon-stimulated genes (ISGs). These data suggested that epithelial cells are protected against viral replication by co-option of two evolutionarily related cytokine networks. These data may inform the design of novel immunotherapy for viral infections that are sensitive to interferons.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ 13/31
/ 14
/ 38
/ 64
/ 64/60
/ Animals
/ Dogs
/ Epithelial Cells - immunology
/ Epithelial Cells - metabolism
/ Gene Expression - drug effects
/ Gene Expression - immunology
/ Humans
/ Intestinal Mucosa - metabolism
/ Madin Darby Canine Kidney Cells
/ Receptors, Cytokine - genetics
/ Receptors, Cytokine - immunology
/ Reverse Transcriptase Polymerase Chain Reaction
/ Rotavirus Infections - genetics
/ Rotavirus Infections - immunology
/ Rotavirus Infections - virology
/ STAT1 Transcription Factor - genetics
/ STAT1 Transcription Factor - immunology
