ArticlePloS one2010
EGR-2 is not required for in vivo CD4 T cell mediated immune responses.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- EGR2 Deletion Suppresses Anti-DsDNA Autoantibody and IL-17 Production in Autoimmune-Prone B6/lpr Mice: A Differential Immune Regulatory Role of EGR2 in B6/lpr Versus Normal B6 Mice.Frontiers in immunology · 2022Article
- Antigen-driven EGR2 expression is required for exhausted CD8Nature communications · 2021Article
- EGR2 is elevated and positively regulates inflammatory IFNγ production in lupus CD4BMC immunology · 2020Article
- Transcription factors early growth response gene (Egr) 2 and 3 control inflammatory responses of tolerant T cells.Immunity, inflammation and disease · 2018Article
- Early Growth Response Gene 2-Expressing CD4Frontiers in immunology · 2018Review
- Egr2 and 3 control adaptive immune responses by temporally uncoupling expansion from T cell differentiation.The Journal of experimental medicine · 2017Article
- Egr2 and 3 Inhibit T-bet-Mediated IFN-γ Production in T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Ndrg1 is a T-cell clonal anergy factor negatively regulated by CD28 costimulation and interleukin-2.Nature communications · 2015Article
- EGR2 is critical for peripheral naïve T-cell differentiation and the T-cell response to influenza.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Transcriptional regulator early growth response gene 2 (Egr2) is required for T cell anergy in vitro and in vivo.The Journal of experimental medicine · 2012Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe zinc finger transcription factor EGR-2 has been shown to play an important role in the induction of T cell anergy and the regulation of peripheral T cell tolerance. In vitro, a prior study has show that T cells deficient in EGR-2 are hyperproliferative to IL-2 and produce elevated levels of the effector cytokine IFN-γ. EGR-2 deficient mice have increased levels of CD44(high) T cells in peripheral lymphoid organs, and with age, develop autoimmune-like features. PRINCIPAL
findingsHere we show that despite increased numbers of cells bearing an activated CD44(high)CD62L(low) phenotype, T cells from young healthy EGR-2 deficient mice have normal proliferative and cytokine responses, and the mice themselves mount normal immune responses against minor histocompatibility antigens, and the pathogens Toxoplasma gondii and lymphocytic choriomeningitis virus.
conclusionsOur results indicate that EGR-2 is not required to mount normal acute in vivo immune responses against foreign antigens, and suggest instead that it may serve to regulate the response to chronic antigenic exposure, such as that which occurs to autoantigens.
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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.