ArticleJournal of autoimmunity2019
Selective deletion of Eos (Ikzf4) in T-regulatory cells leads to loss of suppressive function and development of systemic autoimmunity.
Article in Journal of autoimmunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 63 citations in OpenAlex.
- Maintenance DNA methylation is necessary for age-related alterations in regulatory T cell transcriptional and DNA methylation signatures.bioRxiv : the preprint server for biology · 2026Article
- Aiolos and Eos drive distinct human TH17 functional states.Cellular and molecular life sciences : CMLS · 2026Article
- Eos plays a critical role in Treg homeostasis and modulates the function of recirculating thymic Tregs in the control of Treg development.Cell reports · 2026Article
- CD25Frontiers in immunology · 2026Article
- IKZF-associated inborn errors of immunity.Journal of human immunity · 2025Review
- Article
- Interleukin-2 receptor signaling acts as a checkpoint that influences the distribution of regulatory T cell subsets.iScience · 2024Article
- Novel insights into the pleiotropic health effects of growth differentiation factor 11 gained from genome-wide association studies in population biobanks.BMC genomics · 2024Article
- Infiltrating treg reprogramming in the tumor immune microenvironment and its optimization for immunotherapy.Biomarker research · 2024Review
- Long noncoding RNA LIRIL2R modulates FOXP3 levels and suppressive function of human CD4Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Inferring upstream regulatory genes of FOXP3 in human regulatory T cells from time-series transcriptomic data.NPJ systems biology and applications · 2024Article
- Identification and Functional Analysis of a de novo IKZF3 Mutation in a Pediatric Patient with Combined Immunodeficiency.Journal of clinical immunology · 2024Article
- Article
- Cytotoxic Programming of CD4+ T Cells Is Regulated by Opposing Actions of the Related Transcription Factors Eos and Aiolos.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- IKAROS Family Transcription Factors in Lymphocyte Differentiation and Function.Advances in experimental medicine and biology · 2024Review
- The role of transcription factors in shaping regulatory T cell identity.Nature reviews. Immunology · 2023Review
- Alopecia Areata: A Review of the Genetic Variants and Immunodeficiency Disorders Associated with Alopecia Areata.Skin appendage disorders · 2023Review
- Eos Promotes TH2 Differentiation by Interacting with and Propagating the Activity of STAT5.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Prenatal benzene exposure in mice alters offspring hypothalamic development predisposing to metabolic disease in later life.Chemosphere · 2023Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Eos (lkzf4) is a member of the Ikaros family of transcription factors and is preferentially expressed in T-regulatory (Treg) cells. However, the role of Eos in Treg function is controversial. One study using siRNA knock down of Eos demonstrated that it was critical for Treg suppressor function. In contrast, Treg from mice with a global deficiency of Eos had normal Treg function in vitro and in vivo. To further dissect the function of Eos in Tregs, we generated mice with a conditional knock out of Eos in Treg cells (lkzf4
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Registered trials
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.