ArticleEuropean journal of immunology2015
Premature thymic involution is independent of structural plasticity of the thymic stroma.
Article in European journal of immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Age-related thymic involution: Mechanistic insights and rejuvenating approaches to restore immune function.Science advances · 2026Review
- Comprehensive characterisation of age-related changes in cell subpopulations and tissue structural properties in secondary lymphoid organs.Cell death & disease · 2025Article
- Radiation inducible MafB gene is required for thymic regeneration.Scientific reports · 2021Article
- Acute Myeloid Leukemia: Is It T Time?Cancers · 2021Review
- Distinct organization of adaptive immunity in the long-lived rodent Spalax galili.Nature aging · 2021Article
- Increased epithelial-free areas in thymuses with altered EphB-mediated thymocyte-thymic epithelial cell interactions.Histochemistry and cell biology · 2017Article
- An orthologous non-MHC locus in rats and mice is linked to CD4Genes and immunity · 2017Article
- The cellular composition of the human immune system is shaped by age and cohabitation.Nature immunology · 2016Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
The thymus is the organ devoted to T-cell production. The thymus undergoes multiple rounds of atrophy and redevelopment before degenerating with age in a process known as involution. This process is poorly understood, despite the influence the phenomenon has on peripheral T-cell numbers. Here we have investigated the FVB/N mouse strain, which displays premature thymic involution. We find multiple architectural and cellular features that precede thymic involution, including disruption of the epithelial-endothelial relationship and a progressive loss of pro-T cells. The architectural features, reminiscent of the human thymus, are intrinsic to the nonhematopoietic compartment and are neither necessary nor sufficient for thymic involution. By contrast, the loss of pro-T cells is intrinsic to the hematopoietic compartment, and is sufficient to drive premature involution. These results identify pro-T-cell loss as the main driver of premature thymic involution, and highlight the plasticity of the thymic stroma, capable of maintaining function across diverse interstrain architectures.
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