6533b86dfe1ef96bd12ca8b2
RESEARCH PRODUCT
ID: 213
Peter StaeheliPedro HernandezPedro HernandezAndreas DiefenbachAndreas DiefenbachTanel MahlakõivTanel Mahlakõivsubject
biologymedicine.medical_treatmentImmunologyInnate lymphoid cellHematologyImmunotherapymedicine.disease_causeBiochemistryVirologyInterleukin 22Viral replicationInterferonRotavirusImmunologymedicinebiology.proteinImmunology and AllergySTAT1Molecular BiologyTranscription factormedicine.drugdescription
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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2015-11-01 | Cytokine |