Abstract
Age-associated thymic atrophy results in a decline in T lymphocyte output and has been identified as one of the key events that precede inefficient functioning of the immune system in later life. Thymic atrophy is thought to result from a failure of the thymic microenvironment to support thymopoiesis in old age and recent evidence suggests that a decline in interleukin-7 (IL-7) expression may limit thymocyte development by restricting combinations of survival, proliferation and rearrangement of the TCRβ chain. Using RT-PCR and the RNase protection assay, we show that the expression of IL-7 declines with age. Analysis of Connexin 43 expression, a component molecule of gap junctions, whose function is to connect epithelial cells, does not markedly decline with age. These observations suggest that a decline in IL-7 expression is not matched by a similar loss of epithelial cells. These results in conjunction with other studies lead us to speculate that IL-7 producing MHC class II positive TECs are being replaced by cells that do not have this capacity.
Original language | English |
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Pages (from-to) | 455-463 |
Number of pages | 9 |
Journal | Experimental Gerontology |
Volume | 37 |
Issue number | 2-3 |
Early online date | 24 Dec 2001 |
DOIs | |
Publication status | Published - 3 Jan 2002 |
Externally published | Yes |
Keywords
- Interleukin-7
- Lymphocyte
- Stroma
- Thymocyte
ASJC Scopus subject areas
- Biochemistry
- Ageing
- Molecular Biology
- Genetics
- Endocrinology
- Cell Biology