ArticleNature communications2025
Nr4a1 and Nr4a3 redundantly control clonal deletion and contribute to an anergy-like transcriptome in auto-reactive thymocytes to impose tolerance in mice.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Calibrating T cell responsiveness through interactions with self.Nature reviews. Immunology · 2026Review
- Fibroadipogenic progenitor-secreted prostaglandin E2 coordinates stem cell fate via autocrine and paracrine crosstalk in healthy and dystrophic muscle.Cell death and differentiation · 2026Article
- Congenital cytomegalovirus infection drives oligoclonal expansion of cytotoxic γδ T cells from early fetal progenitors.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Mechanistic Investigation of Vitexin in Ameliorating Ovarian Fibrosis in PCOS Mice via the NR4A1/NLRP3 Signaling Pathway.Metabolites · 2026Article
- Auto-inducible expression of chimeric antigen receptor T cells using the NR4A1 promoter.Immunology and cell biology · 2026Article
- Alleviation of experimental arthritis in SKG mice throughFrontiers in immunology · 2026Article
- Cell-intrinsic CD4 T cell tolerance: a new frontier in therapy?Trends in immunology · 2025Review
- Deconstructing the Thymic Microenvironment Through Genesis to Senescence.Immunological reviews · 2025Review
- Cross-talk between aging resilience pathways and autoimmunity onset.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
The Nr4a nuclear hormone receptors are transcriptionally upregulated in response to antigen recognition by the T cell receptor (TCR) in the thymus and are implicated in clonal deletion, but the mechanisms by which they operate are not clear. Moreover, their role in central tolerance is obscured by redundancy among the Nr4a family members and by their reported functions in Treg generation and maintenance. Here we take advantage of competitive bone marrow chimeras and the OT-II/RIPmOVA model to show that Nr4a1 and Nr4a3 are essential for the upregulation of Bcl2l11/BIM and thymic clonal deletion by self-antigen. Importantly, thymocytes lacking Nr4a1/3 acquire an anergy-like signature after escaping clonal deletion and Treg lineage diversion. We further show that the Nr4a family helps mediate a broad transcriptional program in self-reactive thymocytes that resembles anergy and may operate at the margins of canonical thymic tolerance mechanisms to restrain self-reactive T cells after thymic egress.
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Registered trials
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