ArticleImmunity, inflammation and disease2018
Transcription factors early growth response gene (Egr) 2 and 3 control inflammatory responses of tolerant T cells.
Article in Immunity, inflammation and disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 30 citations in OpenAlex.
- Multifaceted regulatory mechanisms of the EGR family in tumours and prospects for therapeutic applications (Review).International journal of molecular medicine · 2025Review
- Epigenome-Wide Association Studies of the Fractional Exhaled Nitric Oxide and Bronchodilator Drug Response in Moderate-to-Severe Pediatric Asthma.Biomedicines · 2023Article
- The YAP/HIF-1α/miR-182/EGR2 axis is implicated in asthma severity through the control of Th17 cell differentiation.Cell & bioscience · 2021Article
- Small, Dense Low-Density Lipoprotein-Cholesterol and Atherosclerosis: Relationship and Therapeutic Strategies.Frontiers in cardiovascular medicine · 2021Review
- Stepwise Tfh cell differentiation revisited: new advances and long-standing questions.Faculty reviews · 2021Article
- MicroRNA-mediated inflammation and coagulation effects in rats exposed to an inhaled analog of sulfur mustard.Annals of the New York Academy of Sciences · 2020Article
- Egr2 and 3 control inflammation, but maintain homeostasis, of PD-1Life science alliance · 2020Article
- EGR-mediated control of STIM expression and function.Cell calcium · 2019Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
introductionImpaired proliferation and production of IL2 are the hallmarks of experimental T cell tolerance. However, in most autoimmune diseases, auto-reactive T cells do not display hyper proliferation, but inflammatory phenotypes.
methodsWe have now demonstrated that the transcription factors Egr2 and 3 are important for the control of inflammatory cytokine production by tolerant T cells, but not for tolerance induction.
resultsIn the absence of Egr2 and 3, T cell tolerance, as measured by impaired proliferation and production of IL2, can still be induced, but tolerant T cells produced high levels of inflammatory cytokines. Egr2 and 3 regulate expression of differentiation repressors and directly inhibit T-bet function in T cells. Indeed, decreased expression of differentiation repressors, such as Id3 and Tcf1, and increased expression of inflammatory transcription factors, such as RORγt and Bhlhe40 were found in Egr2/3 deficient T cells under tolerogenic conditions. In addition, T-bet was co-expressed with Egr2 in tolerant T cells and Egr2/3 defects leads to production of high levels of IFNγ in tolerant T cells.
conclusionsOur findings demonstrated that despite impaired proliferation and IL2 production, tolerant T cells can display inflammatory responses in response to antigen stimulation and this is controlled at least partly by Egr2 and 3.
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