Age-associated thymic atrophy is not associated with a deficiency in the CD44+CD25-CD3-CD4-CD8- thymocyte population

Richard Aspinall, Deborah Andrew

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

Age-associated thymic atrophy has been proposed to be due to changes in both the thymic microenvironment and in the intrinsic properties of the early T cell progenitors, the CD44+CD25-CD3-CD4-CD8- cells. We have purified these cells from the thymus of both old and young mice and demonstrate no age-associated defect in their ability to differentiate into their progeny in vitro when used to reconstitute fetal thymic organ cultures. We also demonstrate that in the presence of anti-IL-7, CD44+CD25-CD3-CD4-CD8- cells from young mice show reduced thymocyte development in fetal thymic organ cultures compared with controls. Finally we have shown that old mice treated with IL-7 show improved thymopoiesis compared with control groups. The increased thymopoiesis seen in the old animals occurs in the sequential manner which would be anticipated for an agent working directly on the early stages, including the CD44+CD25-CD3-CD4-CD8- cells.

Original languageEnglish
Pages (from-to)150-157
Number of pages8
JournalCellular Immunology
Volume212
Issue number2
DOIs
Publication statusPublished - 15 Sep 2001
Externally publishedYes

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Thymocytes
Atrophy
Interleukin-7
Organ Culture Techniques
Population
Fetal Development
Thymus Gland
T-Lymphocytes
Control Groups

ASJC Scopus subject areas

  • Immunology

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Age-associated thymic atrophy is not associated with a deficiency in the CD44+CD25-CD3-CD4-CD8- thymocyte population. / Aspinall, Richard; Andrew, Deborah.

In: Cellular Immunology, Vol. 212, No. 2, 15.09.2001, p. 150-157.

Research output: Contribution to journalArticle

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