ArticleProceedings of the National Academy of Sciences of the United States of America2022
Redox status regulates autophagy in thymic stromal cells and promotes T cell tolerance.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Multifaceted regulation of thymic tolerance by pattern recognition cascades.Frontiers in immunology · 2026Review
- Redox-Immune Axis and Ozone Pollution: From Oxidative Stress to Thymic Involution and Neurodegeneration.Medical sciences (Basel, Switzerland) · 2025Review
- Paracrine FGF21 dynamically modulates mTOR signaling to regulate thymus function across the lifespan.Nature aging · 2025Article
- Mitochondrial protein C15ORF48 is a stress-independent inducer of autophagy that regulates oxidative stress and autoimmunity.Nature communications · 2024Article
- Autophagy and proteasomes in thymic epithelial cells: essential bulk protein degradation systems for immune homeostasis maintenance.Frontiers in immunology · 2024Review
- Disorganization of secondary lymphoid organs and dyscoordination of chemokine secretion as key contributors to immune aging.Seminars in immunology · 2023Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
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Abstract
Thymic stromal cells (TSCs) are critical regulators of T cell tolerance, but their basic biology has remained under-characterized because they are relatively rare and difficult to isolate. Recent work has revealed that constitutive autophagy in TSCs is required for self-antigen presentation and central T cell tolerance induction; however, the mechanisms regulating constitutive autophagy in TSCs are not well understood. Hydrogen peroxide has been shown to increase autophagy flux in other tissues, and we previously identified conspicuously low expression of the hydrogen peroxide-quenching enzyme catalase in TSCs. We investigated whether the redox status of TSCs established by low catalase expression regulates their basal autophagy levels and their capacity to impose central T cell tolerance. Transgenic overexpression of catalase diminished autophagy in TSCs and impaired thymocyte clonal deletion, concomitant with increased frequencies of spontaneous lymphocytic infiltrates in lung and liver and of serum antinuclear antigen reactivity. Effects on clonal deletion and autoimmune indicators were diminished in catalase transgenic mice when autophagy was rescued by expression of the Becn1
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