期刊
CELL HOST & MICROBE
卷 20, 期 3, 页码 283-295出版社
CELL PRESS
DOI: 10.1016/j.chom.2016.08.003
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资金
- Cancer Research UK
- National Research Foundation of Korea [NRF-2015R1A2A2A09001059]
- Biotechnology and Biological Sciences Research Council
- Empire State Stem Cell Fund through New York State Department of Health NYSTEM contract [C029542]
- Wellcome Trust [Pennetta8920]
- Motor Neuron Disease Association [Pennetta6231]
- Breast Cancer Now [2013MayPR023]
- National Health Service
- Biotechnology and Biological Sciences Research Council [BB/L021684/1] Funding Source: researchfish
- Medical Research Council [G1000089, MR/M019217/1] Funding Source: researchfish
- BBSRC [BB/L021684/1] Funding Source: UKRI
- MRC [MR/M019217/1, G1000089] Funding Source: UKRI
Pattern recognition receptors are activated following infection and trigger transcriptional programs important for host defense. Tight regulation of NF-kappa B activation is critical to avoid detrimental and misbalanced responses. We describe Pickle, a Drosophila nuclear I kappa B that integrates signaling inputs from both the Imd and Toll pathways by skewing the transcriptional output of the NF-kappa B dimer repertoire. Pickle interacts with the NF-kappa B protein Relish and the histone deacetylase dHDAC1, selectively repressing Relish homodimers while leaving other NF-kappa B dimer combinations unscathed. Pickle's ability to selectively inhibit Relish homodimer activity contributes to proper host immunity and organismal health. Although loss of pickle results in hyper-induction of Relish target genes and improved host resistance to pathogenic bacteria in the short term, chronic inactivation of pickle causes loss of immune tolerance and shortened lifespan. Pickle therefore allows balanced immune responses that protect from pathogenic microbes while permitting the establishment of beneficial commensal hostmicrobe relationships.
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