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Interleukin-2 enhances CD4(+) T cell memory by promoting the generation of IL-7Rα–expressing cells

The common γ chain cytokines interleukin (IL)-2 and IL-7 are important regulators of T cell homeostasis. Although IL-2 is implicated in the acute phase of the T cell response, IL-7 is important for memory T cell survival. We asked whether regulated responsiveness to these growth factors is determine...

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Detalles Bibliográficos
Autores principales: Dooms, Hans, Wolslegel, Kristen, Lin, Patricia, Abbas, Abul K.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2137906/
https://www.ncbi.nlm.nih.gov/pubmed/17312008
http://dx.doi.org/10.1084/jem.20062381
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author Dooms, Hans
Wolslegel, Kristen
Lin, Patricia
Abbas, Abul K.
author_facet Dooms, Hans
Wolslegel, Kristen
Lin, Patricia
Abbas, Abul K.
author_sort Dooms, Hans
collection PubMed
description The common γ chain cytokines interleukin (IL)-2 and IL-7 are important regulators of T cell homeostasis. Although IL-2 is implicated in the acute phase of the T cell response, IL-7 is important for memory T cell survival. We asked whether regulated responsiveness to these growth factors is determined by temporal expression of the cytokine-specific IL-2 receptor (R) α and IL-7Rα chains. We demonstrate that IL-2Rα is expressed early after priming in T cell receptor–transgenic CD4(+) T cells, whereas IL-7Rα expression is lost. In the later stage of the response, IL-7Rα is reexpressed while IL-2Rα expression is silenced. This reciprocal pattern of IL-2Rα/IL-7Rα expression is disturbed when CD4(+) T cells are primed in the absence of IL-2 signals. Primed IL-2(−/−) or CD25(−/−) (IL-2Rα(−/−)) CD4(+) T cells, despite showing normal induction of activation markers and cell division, fail to reexpress IL-7Rα late in the response. Because the generation of CD4(+) memory T cells is dependent on IL-7–IL-7Rα interactions, primed IL-2(−/−) or CD25(−/−) CD4(+) T cells develop poorly into long-lived memory cells. Retrovirus-mediated expression of IL-7Rα in IL-2(−/−) T cells restores their capacity for long-term survival. These results identify IL-2 as a factor regulating IL-7Rα expression and, consequently, memory T cell homeostasis in vivo.
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spelling pubmed-21379062007-12-13 Interleukin-2 enhances CD4(+) T cell memory by promoting the generation of IL-7Rα–expressing cells Dooms, Hans Wolslegel, Kristen Lin, Patricia Abbas, Abul K. J Exp Med Articles The common γ chain cytokines interleukin (IL)-2 and IL-7 are important regulators of T cell homeostasis. Although IL-2 is implicated in the acute phase of the T cell response, IL-7 is important for memory T cell survival. We asked whether regulated responsiveness to these growth factors is determined by temporal expression of the cytokine-specific IL-2 receptor (R) α and IL-7Rα chains. We demonstrate that IL-2Rα is expressed early after priming in T cell receptor–transgenic CD4(+) T cells, whereas IL-7Rα expression is lost. In the later stage of the response, IL-7Rα is reexpressed while IL-2Rα expression is silenced. This reciprocal pattern of IL-2Rα/IL-7Rα expression is disturbed when CD4(+) T cells are primed in the absence of IL-2 signals. Primed IL-2(−/−) or CD25(−/−) (IL-2Rα(−/−)) CD4(+) T cells, despite showing normal induction of activation markers and cell division, fail to reexpress IL-7Rα late in the response. Because the generation of CD4(+) memory T cells is dependent on IL-7–IL-7Rα interactions, primed IL-2(−/−) or CD25(−/−) CD4(+) T cells develop poorly into long-lived memory cells. Retrovirus-mediated expression of IL-7Rα in IL-2(−/−) T cells restores their capacity for long-term survival. These results identify IL-2 as a factor regulating IL-7Rα expression and, consequently, memory T cell homeostasis in vivo. The Rockefeller University Press 2007-03-19 /pmc/articles/PMC2137906/ /pubmed/17312008 http://dx.doi.org/10.1084/jem.20062381 Text en Copyright © 2007, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Articles
Dooms, Hans
Wolslegel, Kristen
Lin, Patricia
Abbas, Abul K.
Interleukin-2 enhances CD4(+) T cell memory by promoting the generation of IL-7Rα–expressing cells
title Interleukin-2 enhances CD4(+) T cell memory by promoting the generation of IL-7Rα–expressing cells
title_full Interleukin-2 enhances CD4(+) T cell memory by promoting the generation of IL-7Rα–expressing cells
title_fullStr Interleukin-2 enhances CD4(+) T cell memory by promoting the generation of IL-7Rα–expressing cells
title_full_unstemmed Interleukin-2 enhances CD4(+) T cell memory by promoting the generation of IL-7Rα–expressing cells
title_short Interleukin-2 enhances CD4(+) T cell memory by promoting the generation of IL-7Rα–expressing cells
title_sort interleukin-2 enhances cd4(+) t cell memory by promoting the generation of il-7rα–expressing cells
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2137906/
https://www.ncbi.nlm.nih.gov/pubmed/17312008
http://dx.doi.org/10.1084/jem.20062381
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