Type III IFNS are commonly induced by bacteria-sensing TLRS and reinforce epithelial barriers during infection

Charlotte Odendall, Andrew A. Voak, Jonathan C. Kagan*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

69 Citations (Scopus)

Abstract

Type III IFNs (IFN-ls) are secreted factors that are well-known for their antiviral activities. However, their regulation and functions during bacterial infections are unclear. In this article, we report that the regulation of IFN-l genes did not track with mechanisms that control type I IFN expression in response to TLRs. Whereas type I IFNs were only expressed from TLRs present on endosomes, type III IFNs could be induced by TLRs that reside at the plasma membrane and that detect various bacterial products. The mechanisms that regulate type III IFN gene expression tracked with those that promote inflammatory cytokine and chemokine expression. Importantly, rIFN-ls enhanced epithelial barriers in vitro, preventing transcellular bacteria dissemination. We therefore propose that in addition to their functions in cell-intrinsic antiviral immunity, type III IFNs protect epithelial barrier integrity, an activity that would benefit the host during any infectious encounter.

Original languageEnglish
Pages (from-to)3271-3279
Number of pages9
JournalJournal of Immunology
Volume199
Issue number9
Early online date1 Nov 2017
DOIs
Publication statusPublished - 1 Nov 2017

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