ArticleNature communications2014
The Menin-Bach2 axis is critical for regulating CD4 T-cell senescence and cytokine homeostasis.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 96 citations in OpenAlex.
- Building an Interleukin-10-Producing Identity: How B Cells Acquire Interleukin-10 Competence and How Plasma Cell Differentiation Consolidates This Program.Immunological reviews · 2026Review
- How age and sex interaction is associated with immune aging with implications for vaccines and age-related autoimmunity.npj aging · 2026Review
- Ligature-induced periodontitis in mice potentially accelerates CD4Frontiers in immunology · 2026Article
- BACH2 drives the development and function of group 2 innate lymphoid cells.Science advances · 2025Article
- Meta-epigenetic shifts in T cell aging and aging-related dysfunction.Journal of biomedical science · 2025Review
- Dysregulation of the tumor suppressor Menin and its target Bach2 in HTLV-1 infection.Retrovirology · 2025Article
- An in-depth understanding of the role and mechanisms of T cells in immune organ aging and age-related diseases.Science China. Life sciences · 2025Review
- Cellular senescence by loss of Men1 in osteoblasts is critical for age-related osteoporosis.Aging cell · 2024Article
- MEN1 deficiency stabilizes PD-L1 and promotes tumor immune evasion of lung cancer.Cancer science · 2024Article
- The role of Bach2 in regulating CD8 + T cell development and function.Cell communication and signaling : CCS · 2024Review
- Spatial profiling reveals tissue-specific neuro-immune interactions in gastroenteropancreatic neuroendocrine tumors.The Journal of pathology · 2024Article
- Chromatin conformational changes at human satellite II contribute to the senescence phenotype in the tumor microenvironment.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Senescent CD8Cancer science · 2023Article
- Article
- Immune Memory in Aging: a Wide Perspective Covering Microbiota, Brain, Metabolism, and Epigenetics.Clinical reviews in allergy & immunology · 2022Review
- Menin directs regionalized decidual transformation through epigenetically setting PTX3 to balance FGF and BMP signaling.Nature communications · 2022Article
- Tumour burden and efficacy of immune-checkpoint inhibitors.Nature reviews. Clinical oncology · 2022Review
- Article
- A CRISPR/Cas9-mediated screen identifies determinants of early plasma cell differentiation.Frontiers in immunology · 2022Article
- Protections of transcription factor BACH2 and natural product myricetin against pathological cardiac hypertrophy and dysfunction.Frontiers in physiology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although CD4 T-cell senescence plays an important role in immunosenescence, the mechanism behind this process remains unclear. Here we show that T cell-specific Menin deficiency results in the premature senescence of CD4 T cells, which is accompanied by the senescence-associated secretory phenotype after antigenic stimulation and dysregulated cytokine production. Menin is required for the expansion and survival of antigen-stimulated CD4 T cells in vivo and acts by targeting Bach2, which is known to regulate immune homeostasis and cytokine production. Menin binds to the Bach2 locus and controls its expression through maintenance of histone acetylation. Menin binding at the Bach2 locus and the Bach2 expression are decreased in the senescent CD4 T cells. These findings reveal a critical role of the Menin-Bach2 pathway in regulating CD4 T-cell senescence and cytokine homeostasis, thus indicating the involvement of this pathway in the inhibition of immunosenescence.
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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.