ArticleThe Journal of experimental medicine2024
Eomes-dependent mitochondrial regulation promotes survival of pathogenic CD4+ T cells during inflammation.
Article in The Journal of experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- CAR signaling instructs divergent metabolic reprogramming and functional fates in αβ and γδ T cells.Cellular & molecular immunology · 2026Article
- The immunology behind inflammaging-causes, sources, and mechanisms.The Journal of allergy and clinical immunology · 2026Review
- A unique CD4⁺ T cell subset expressing granzyme K is regulated by transcription factor EOMES and important for T cell-mediated intestinal inflammation.Nature immunology · 2026Article
- Peptide nanofibers and PAMP agonist combinations enhance pulmonary CD4Journal of nanobiotechnology · 2026Article
- VNUT-mediated ATP release suppresses T helper 1 (TScience advances · 2025Article
- CD4 T cells acquire Eomesodermin to modulate cellular senescence and aging.Nature aging · 2025Article
- Mitochondria and lysosomes in T cell immunometabolism.Trends in immunology · 2025Review
- A new method to measure cell metabolism of rare cells in vivo reveals a high oxidative phosphorylation dependence of lung T cells.Immunology and cell biology · 2025Article
- CD1d-Restricted NKT Cells Promote Central Memory CD8International journal of molecular sciences · 2025Article
- Metabolic checkpoints in rheumatoid arthritis.Seminars in arthritis and rheumatism · 2025Review
- Eomesodermin-expressing CD4 Th cells and association with multiple sclerosis progression and brain atrophy.Brain communications · 2025Article
- NF-κB subunits RelA and c-Rel selectively control CD4+ T cell function in multiple sclerosis and cancer.The Journal of experimental medicine · 2024Article
- Cytokine Storm Related to CD4Immune network · 2024Article
Corrections and comments
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Authors and funding
21 authors at 5 institutions in 2 countries.
Funding
Abstract
The mechanisms whereby Eomes controls tissue accumulation of T cells and strengthens inflammation remain ill-defined. Here, we show that Eomes deletion in antigen-specific CD4+ T cells is sufficient to protect against central nervous system (CNS) inflammation. While Eomes is dispensable for the initial priming of CD4+ T cells, it is required for long-term maintenance of CNS-infiltrating CD4+ T cells. We reveal that the impact of Eomes on effector CD4+ T cell longevity is associated with sustained expression of multiple genes involved in mitochondrial organization and functions. Accordingly, epigenetic studies demonstrate that Eomes supports mitochondrial function by direct binding to either metabolism-associated genes or mitochondrial transcriptional modulators. Besides, the significance of these findings was confirmed in CD4+ T cells from healthy donors and multiple sclerosis patients. Together, our data reveal a new mechanism by which Eomes promotes severity and chronicity of inflammation via the enhancement of CD4+ T cell mitochondrial functions and resistance to stress-induced cell death.
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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.