期刊
PLOS ONE
卷 9, 期 1, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0083391
关键词
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资金
- National Institutes of Health (NIH) [U01AA018663, P50AA11199, R24AA12885]
- Newcastle Biomedical Research Centre
- Wellcome Trust [WT086755MA]
- Medical Research Council [MK/K001949/1, G0700890]
- European Commission FP7 program grant 'INFLA-CARE' (EC) [223151]
- MRC [G0700890, MR/K001949/1] Funding Source: UKRI
- Medical Research Council [MR/K001949/1, G0700890] Funding Source: researchfish
Toll-like Receptor 3 (TLR3) is a pathogen pattern recognition receptor that plays a key role in innate immunity. TLR3 signalling has numerous functions in liver, both in health and disease. Here we report that TLR3 is expressed by quiescent hepatic stellate cells (HSC) where it functions to induce transcription and secretion of functional interferons as well as a number of other cytokines and chemokines. Upon transdifferentiation into myofibroblasts, HSCs rapidly loose the ability to produce interferon gamma (IFN gamma). Mechanistically, this gene silencing may be due to Polycomb complex mediated repression via methylation of histone H3 lysine 27. In contrast to wild type, quiescent HSC isolated from tlr3 knockout mice do not produce IFN gamma in response to Poly(I:C) treatment. Therefore, quiescent HSC may contribute to induction of the hepatic innate immune system in response to injury or infection.
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