ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Twist1 and Twist2 Contribute to Cytokine Downregulation following Chronic NOD2 Stimulation of Human Macrophages through the Coordinated Regulation of Transcriptional Repressors and Activators.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Novel Experimental Approach to Investigate Immune Control of Vascular Function: Co-culture of Murine Aortas With T Lymphocytes or Macrophages.Bio-protocol · 2025Article
- Acute Shear Stress Induces TWIST-Mediated EndMT in Venous Endothelial Cells and Human Long Saphenous Veins.Cells · 2025Article
- BACH2 regulates diversification of regulatory and proinflammatory chromatin states in TNature immunology · 2024Article
- Gravidity influences distinct transcriptional profiles of maternal and fetal placental macrophages at term.Frontiers in immunology · 2024Article
- Twist1-IRF9 Interaction Is Necessary for IFN-Stimulated Gene Anti-Zika Viral Infection.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Revisiting the Mesenchymal "Stem vs. Stromal" Cell Dichotomy and Its Implications for Development of Improved Potency Metrics.Stem cells (Dayton, Ohio) · 2023Review
- Pattern Recognition Receptor Signaling and Cytokine Networks in Microbial Defenses and Regulation of Intestinal Barriers: Implications for Inflammatory Bowel Disease.Gastroenterology · 2022Review
- Twist1 in podocytes ameliorates podocyte injury and proteinuria by limiting CCL2-dependent macrophage infiltration.JCI insight · 2021Article
- BMI1 regulates multiple myeloma-associated macrophage's pro-myeloma functions.Cell death & disease · 2021Article
- Human Papillomavirus 16 (HPV16) E2 Repression of TWIST1 Transcription Is a Potential Mediator of HPV16 Cancer Outcomes.mSphere · 2020Article
- Twist1: A Double-Edged Sword in Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2020Review
- The transcription factor Twist1 in the distal nephron but not in macrophages propagates aristolochic acid nephropathy.Kidney international · 2020Article
- Twist1 and Twist2 Induce Human Macrophage Memory upon Chronic Innate Receptor Treatment by HDAC-Mediated Deacetylation of Cytokine Promoters.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Systems genetics identifies a macrophage cholesterol network associated with physiological wound healing.JCI insight · 2019Article
- The Role of IL-10 in Malaria: A Double Edged Sword.Frontiers in immunology · 2019Review
- Genome-wide DNA methylation analysis in jejunum of Sus scrofa with intrauterine growth restriction.Molecular genetics and genomics : MGG · 2018Article
Corrections and comments
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3 authors at 1 institution in 1 country.
Funding
Abstract
Proper regulation of microbial-induced cytokines is critical to intestinal immune homeostasis. Acute stimulation of nucleotide-binding oligomerization domain 2 (NOD2), the Crohn's disease-associated sensor of bacterial peptidoglycan, induces cytokines. However, chronic NOD2 stimulation in macrophages decreases cytokines upon pattern recognition receptor (PRR) restimulation; cytokine attenuation to PRR stimulation is similarly observed in intestinal macrophages. The role for the transcriptional repressors Twist1 and Twist2 in regulating PRR-induced cytokine outcomes is poorly understood and has not been reported for NOD2. We found that Twist1 and Twist2 were required for optimal cytokine downregulation during acute and, particularly, chronic NOD2 stimulation of human macrophages. Consistently, Twist1 and Twist2 expression was increased after chronic NOD2 stimulation; this increased expression was IL-10 and TGF-β dependent. Although Twist1 and Twist2 did not coregulate each other's expression, they cooperated to enhance binding to cytokine promoters after chronic NOD2 stimulation. Moreover, Twist1 and Twist2 contributed to enhance expression and promoter binding of the proinflammatory inhibitor c-Maf and the transcriptional repressor Bmi1. Restoring c-Maf and Bmi1 expression in Twist-deficient macrophages restored NOD2-induced cytokine downregulation. Furthermore, with chronic NOD2 stimulation, Twist1 and Twist2 contributed to the decreased expression and cytokine promoter binding of the transcriptional activators activating transcription factor 4, C/EBPα, Runx1, and Runx2. Knockdown of these transcriptional activators in Twist-deficient macrophages restored cytokine downregulation after chronic NOD2 stimulation. Finally, NOD2 synergized with additional PRRs to increase Twist1 and Twist2 expression and Twist-dependent pathways. Therefore, after chronic NOD2 stimulation Twist1 and Twist2 coordinate the regulation of both transcriptional activators and repressors, thereby mediating optimal cytokine downregulation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.