期刊
EMBO JOURNAL
卷 39, 期 14, 页码 -出版社
WILEY
DOI: 10.15252/embj.2019103454
关键词
IL-10; IL-1beta; macrophages; prostacyclin
资金
- Wellcome Trust [108045/Z/15/Z, 103973/Z/14/Z, 107964/Z/15/Z]
- UK Dementia Research Institute
- Sir Henry Dale Fellowship - Wellcome Trust [099953/Z/12/Z]
- Sir Henry Dale Fellowship - Royal Society [099953/Z/12/Z]
- Wellcome Trust [099953/Z/12/Z, 103973/Z/14/Z] Funding Source: Wellcome Trust
- BBSRC [BB/T009543/1] Funding Source: UKRI
- MRC [UKDRI-3001, G0601617] Funding Source: UKRI
The alarm cytokine interleukin-1 beta (IL-1 beta) is a potent activator of the inflammatory cascade following pathogen recognition. IL-1 beta production typically requires two signals: first, priming by recognition of pathogen-associated molecular patterns leads to the production of immature pro-IL-1 beta; subsequently, inflammasome activation by a secondary signal allows cleavage and maturation of IL-1 beta from its pro-form. However, despite the important role of IL-1 beta in controlling local and systemic inflammation, its overall regulation is still not fully understood. Here we demonstrate that peritoneal tissue-resident macrophages use an active inhibitory pathway, to suppress IL-1 beta processing, which can otherwise occur in the absence of a second signal. Programming by the transcription factor Gata6 controls the expression of prostacyclin synthase, which is required for prostacyclin production after lipopolysaccharide stimulation and optimal induction of IL-10. In the absence of secondary signal, IL-10 potently inhibits IL-1 beta processing, providing a previously unrecognized control of IL-1 beta in tissue-resident macrophages.
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