Premature thymic involution is independent of structural plasticity of the thymic stroma. Issue 5 (23rd February 2015)

• Record Type: Journal Article
• Authors: Franckaert, Dean; Schlenner, Susan M.; Heirman, Nathalie; Gill, Jason; Skogberg, Gabriel; Ekwall, Olov; Put, Karen; Linterman, Michelle A.; Dooley, James; Liston, Adrian
• Is Part Of: European journal of immunology. Volume 45:Issue 5(2015:May)
• Page Start: 1535
• Page End: 1547
• Publication Date: 2015-02-23
• Subjects: Immunology -- Periodicals; 616.079
• DOI: 10.1002/eji.201445277
• Languages: English
• ISSNs: 0014-2980

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>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.</p> </abstract>