Holding the inflammatory system in check: NLRs keep it cool.
Sushmita Jha,Jenny P.-Y. Ting +1 more
TLDR
This report aims to review the literature regarding several members of the nucleotide-binding domain, leucine-rich repeat-containing receptor (NLR) family of pattern recognition sensors/receptors that serve as checkpoints for inflammation.Abstract:
Inflammation is a double-edged sword. While short-lived, acute inflammation is essential for the repair and resolution of infection and damage, uncontrolled and unresolved chronic inflammation is central to several diseases, including cancer, autoimmune diseases, allergy, metabolic disease, and cardiovascular disease. This report aims to review the literature regarding several members of the nucleotide-binding domain, leucine-rich repeat-containing receptor (NLR) family of pattern recognition sensors/receptors that serve as checkpoints for inflammation. Understanding the negative regulation of inflammation is highly relevant to the development of therapeutics for inflammatory as well as infectious diseases.read more
Citations
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NLR-Dependent Regulation of Inflammation in Multiple Sclerosis
Marjan Gharagozloo,Katsiaryna V. Gris,Tara M. Mahvelati,Abdelaziz Amrani,John R. Lukens,Denis Gris +5 more
TL;DR: A summary of the role of NLRs in the pathogenesis of MS is provided and how anti-inflammatory NLRs regulate the immune response within the CNS is summarized.
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Inflammatory pathway genes associated with inter-individual variability in the trajectories of morning and evening fatigue in patients receiving chemotherapy.
Fay Wright,Marilyn J. Hammer,Steven M. Paul,Bradley E. Aouizerat,Kord M. Kober,Yvette P. Conley,Bruce A. Cooper,Laura B. Dunn,Jon D. Levine,Gail D'Eramo Melkus,Christine Miaskowski +10 more
TL;DR: Findings add to the growing body of evidence that suggests that morning and evening fatigue are distinct symptoms.
Journal ArticleDOI
Modeling-Enabled Characterization of Novel NLRX1 Ligands
Pinyi Lu,Raquel Hontecillas,Vida Abedi,Shiv D. Kale,Andrew Leber,Chase Heltzel,Mark Langowski,Victoria Godfrey,Casandra Philipson,Nuria Tubau-Juni,Adria Carbo,Stephen E. Girardin,Aykut Üren,Josep Bassaganya-Riera +13 more
TL;DR: The findings showed that the regulatory function of PUA on colitis is NLRX1 dependent and identified novel small molecules that bind to NLRx1 and exert anti-inflammatory actions.
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Host inflammatory responses to intracellular invaders: Review study
TL;DR: Inflammasome components assemble and oligomerizes leading to the auto cleavage of the pro-caspase-1 to its active form and controls the establishment of the pathogen by mounting inflammatory response and activation of the pyroptotic cell death.
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S1PR1 expression correlates with inflammatory responses to Newcastle disease virus infection
Yaling Li,Peng Xie,Minhua Sun,Bin Xiang,Yinfeng Kang,Pei Gao,Wenxian Zhu,Zhangyong Ning,Tao Ren +8 more
TL;DR: A direct correlation between chicken embryo fibroblast (CEF) cellular inflammatory responses and S1PR1 expression is observed and highlights the important role of S1 PR1 in inflammatory responses in NDV infection.
References
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The Mitochondrial Proteins NLRX1 and TUFM Form a Complex that Regulates Type I Interferon and Autophagy
Yu Lei,Haitao Wen,Yanbao Yu,Debra J. Taxman,Lu Zhang,Douglas G. Widman,Karen V. Swanson,Kwun Wah Wen,Blossom Damania,Christopher Brooks Moore,Patrick M. Giguère,David P. Siderovski,John Hiscott,Babak Razani,Clay F. Semenkovich,Xian Chen,Jenny P.-Y. Ting +16 more
TL;DR: This study establishes a link between an NLR protein and the viral-induced autophagic machinery via an intermediary partner, TUFM, which has similar functions as NLRX1 by inhibiting RLR-induced IFN-I but promoting autophagy.
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NLRP4 negatively regulates type I interferon signaling by targeting the kinase TBK1 for degradation via the ubiquitin ligase DTX4
Jun Cui,Yinyin Li,Yinyin Li,Yinyin Li,Liang Zhu,Dan Liu,Zhou Songyang,Helen Yicheng Wang,Helen Yicheng Wang,Rongfu Wang,Rongfu Wang,Rongfu Wang +11 more
TL;DR: This work reports that the pattern-recognition receptor NLRP4 regulated the activation of type I interferon mediated by double-stranded RNA or DNA by targeting the kinase TBK1 for degradation.
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NLRC3, a Member of the NLR Family of Proteins, Is a Negative Regulator of Innate Immune Signaling Induced by the DNA Sensor STING
Lu Zhang,Jinyao Mo,Karen V. Swanson,Haitao Wen,Alex Petrucelli,Sean M. Gregory,Zhigang Zhang,Monika Schneider,Yan Jiang,Katherine A. Fitzgerald,Songying Ouyang,Zhi-Jie Liu,Blossom Damania,Hong-Bing Shu,Joseph A. Duncan,Jenny P.-Y. Ting +15 more
TL;DR: The nucleotide-binding, leucine-rich-repeat-containing protein, NLRC3, reduced STING-dependent innate immune activation in response to cytosolic DNA, cyclic di-GMP (c-di-G MP), and DNA viruses.
Journal ArticleDOI
NLRC5 Limits the Activation of Inflammatory Pathways
TL;DR: The identification and characterization of NLRC5, a NLR protein whose expression is found predominantly in cells of the myeloid and lymphoid lineages, is presented, and it is identified as a negative modulator of inflammatory pathways.
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The CATERPILLER Protein Monarch-1 Is an Antagonist of Toll-like Receptor-, Tumor Necrosis Factor α-, and Mycobacterium tuberculosis-induced Pro-inflammatory Signals
Kristi L. Williams,John D. Lich,Joseph A. Duncan,William Reed,Prasad Rallabhandi,Chris B. Moore,Sherry Kurtz,V. McNeil Coffield,Mary Ann Accavitti-Loper,Lishan Su,Stefanie N. Vogel,Miriam Braunstein,Jenny P.-Y. Ting +12 more
TL;DR: This work finds that Monarch-1 associates with IRAK-1 but not MyD88, resulting in the blockage of IRAk-1 hyperphosphorylation, the first example of a CLR protein that antagonizes inflammatory responses initiated by TLR agonists via interference with IRAB-1 activation.