The origins of monasticism

O'Neill, Jane

doi:10.1017/cbo9780511555350.017

Cited by 5 publications

(1 citation statement)

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“…Recognition of specific patterns of microbial components by Toll-like receptors (TLRs) in the body leads to activation of innate immunity against pathogens [1][2][3]. TLR3 recognizes dsRNA generated during viral infection and activation of TLR3 results in induction of type I interferons (IFNs), including IFN-b and IFN-a family cytokines, which are crucial mediators of the cellular anti-viral response.…”

Section: Introductionmentioning

confidence: 99%

A20 is a potent inhibitor of TLR3‐ and Sendai virus‐induced activation of NF‐κB and ISRE and IFN‐β promoter

et al. 2004

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Toll-like receptor 3 (TLR3) recognizes dsRNA generated during viral infection and activation of TLR3 results in induction of type I interferons (IFNs) and cellular anti-viral response. TLR3 is associated with a TIR domain-containing adapter protein TRIF, which activates distinct downstream pathways leading to activation of NF-jB and ISRE sites in the promoters of type I IFNs. We show here that A20, a NF-jBinducible zinc finger protein that has been demonstrated to be an inhibitor of TNF-induced NF-jB activation and a physiological suppressor of inflammatory response, potently inhibited TLR3-and Sendai virus-mediated activation of ISRE and NF-jB and IFN-b promoter in reporter gene assays. A20 also inhibited TRIF-, but not its downstream signaling components TBK1-, IKKb-, and IKKe-mediated activation of ISRE and NF-jB and IFN-b promoter. Moreover, A20 interacted with TRIF in coimmunoprecipitation experiments. Finally, expression of A20 could be induced at protein level by Sendai virus infection. These data suggest that A20 targets TRIF to inhibit TLR3-mediated induction of IFN-b transcription and functions as a feedback negative regulator for TLR3 signaling and cellular anti-viral response.

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Section: Introductionmentioning

confidence: 99%