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10.4049/jimmunol.1700250

http://scihub22266oqcxt.onion/10.4049/jimmunol.1700250
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C5679450!5679450!28954888
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suck abstract from ncbi


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pmid28954888      J+Immunol 2017 ; 199 (9): 3270-9
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  • Type III interferons are commonly induced by bacteria-sensing TLRs, and reinforce epithelial barriers during infection #MMPMID28954888
  • Odendall C; Voak AA; Kagan JC
  • J Immunol 2017[Nov]; 199 (9): 3270-9 PMID28954888show ga
  • Type III interferons (IFN?s) are secreted factors that are well-known for their antiviral activities. However, their regulation and functions during bacterial infections are unclear. Herein, we report that the regulation of IFN? genes did not track with mechanisms that control type I IFN expression in response to Toll-like Receptors (TLRs). While 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, recombinant IFN?s 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.
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