Age-associated thymic atrophy is linked to a decline in IL-7 production

Deborah Andrew, Richard Aspinall

Research output: Contribution to journalArticle

124 Citations (Scopus)

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 languageEnglish
Pages (from-to)455-463
Number of pages9
JournalExperimental Gerontology
Volume37
Issue number2-3
Early online date24 Dec 2001
DOIs
Publication statusPublished - 3 Jan 2002
Externally publishedYes

Fingerprint

Interleukin-7
Atrophy
Epithelial Cells
Connexin 43
T-cells
Immune system
Gap Junctions
Thymocytes
Ribonucleases
Immune System
Assays
T-Lymphocytes
Polymerase Chain Reaction
Molecules

Keywords

  • Interleukin-7
  • Lymphocyte
  • Stroma
  • Thymocyte

ASJC Scopus subject areas

  • Biochemistry
  • Ageing
  • Molecular Biology
  • Genetics
  • Endocrinology
  • Cell Biology

Cite this

Age-associated thymic atrophy is linked to a decline in IL-7 production. / Andrew, Deborah; Aspinall, Richard.

In: Experimental Gerontology, Vol. 37, No. 2-3, 03.01.2002, p. 455-463.

Research output: Contribution to journalArticle

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