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Interleukin (il)-15 and il-7 jointly regulate homeostatic proliferation of memory phenotype cd8(+) cells but are not required for memory phenotype cd4(+) cells

Academic Article
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Overview

authors

  • Tan, J. T.
  • Ernst, B.
  • Kieper, W. C.
  • LeRoy, E.
  • Sprent, Jonathan
  • Surh, Charles

publication date

  • 2002

journal

  • Journal of Experimental Medicine  Journal

abstract

  • The overall size and composition of the pool of naive and memory T cells are tightly regulated by homeostatic mechanisms. Recent work has shown that homeostasis of naive T cells is controlled by two factors, self-major histocompatibility complex (MHC)/peptide ligands and a cytokine, interleukin (IL)-7. In particular, contact with these two factors is required for naive CD4+ and CD8+ cells to undergo "homeostatic" proliferation, i.e., proliferation induced as a consequence of severe T cell depletion. In contrast to naive T cells, the factors that drive memory T cells to undergo homeostatic proliferation are poorly understood. To address this issue, purified memory phenotype CD4+ and CD8+ cells from normal mice were adoptively transferred into various gene-knockout mice rendered T cell-deficient by sublethal irradiation. Three findings are reported. First, unlike naive T cells, homeostatic proliferation of memory T cells is largely MHC independent. Second, memory CD8+ cells can utilize either IL-7 or IL-15 to undergo homeostatic proliferation; however, in the absence of both IL-7 and IL-15, homeostatic proliferation fails to occur. Third, unlike memory CD8+ cells, homeostatic proliferation of memory CD4+ cells is independent of IL-7 and IL-15 (also IL-4). Thus, the homeostatic proliferation mechanisms that control memory CD8+ cells and memory CD4+ cells are quite distinct.

subject areas

  • Animals
  • CD4-Positive T-Lymphocytes
  • CD8-Positive T-Lymphocytes
  • Cell Division
  • Homeostasis
  • Immunologic Memory
  • Immunophenotyping
  • Interleukin-15
  • Interleukin-7
  • Mice
  • Mice, Knockout
  • Mice, Transgenic
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Identity

PubMed Central ID

  • PMC2193564

International Standard Serial Number (ISSN)

  • 0022-1007

Digital Object Identifier (DOI)

  • 10.1084/jem.20020066

PubMed ID

  • 12070280
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Additional Document Info

start page

  • 1523

end page

  • 1532

volume

  • 195

issue

  • 12

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