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Treatment with Soluble Interleukin-15Rα Exacerbates Intracellular Parasitic Infection by Blocking the Development of Memory CD8(+) T Cell Response
Interferon (IFN)-γ–producing CD8(+) T cells are important for the successful resolution of the obligate intracellular parasite Toxoplasma gondii by preventing the reactivation or controlling a repeat infection. Previous reports from our laboratory have shown that exogenous interleukin (IL)-15 treatm...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2002
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193543/ https://www.ncbi.nlm.nih.gov/pubmed/12045244 http://dx.doi.org/10.1084/jem.20011915 |
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author | Khan, Imtiaz A. Moretto, Magali Wei, Xiao-qing Williams, Martha Schwartzman, Joseph D. Liew, Foo Y. |
author_facet | Khan, Imtiaz A. Moretto, Magali Wei, Xiao-qing Williams, Martha Schwartzman, Joseph D. Liew, Foo Y. |
author_sort | Khan, Imtiaz A. |
collection | PubMed |
description | Interferon (IFN)-γ–producing CD8(+) T cells are important for the successful resolution of the obligate intracellular parasite Toxoplasma gondii by preventing the reactivation or controlling a repeat infection. Previous reports from our laboratory have shown that exogenous interleukin (IL)-15 treatment augments the CD8(+) T cell response against the parasite. However, the role of endogenous IL-15 in the proliferation of activated/memory CD8(+) T cells during toxoplasma or any other infection is unknown. In this study, we treated T. gondii immune mice with soluble IL-15 receptor α (sIL-15Rα) to block the host endogenous IL-15. The treatment markedly reduced the ability of the immune animals to control a lethal infection. CD8(+) T cell activities in the sIL-15Rα–administered mice were severely reduced as determined by IFN-γ release and target cell lysis assays. The loss of CD8(+) T cell immunity due to sIL-15Rα treatment was further demonstrated by adoptive transfer experiments. Naive recipients transferred with CD44(hi) activated/memory CD8(+) T cells and treated with sIL-15Rα failed to resist a lethal T. gondii infection. Moreover, sIL-15Rα treatment of the recipients blocked the ability of donor CD44(hi) activated/memory CD8(+) T cells to replicate in response to T. gondii challenge. To our knowledge, this is the first demonstration of the important role of host IL-15 in the development of antigen-specific memory CD8(+) T cells against an intracellular infection. |
format | Text |
id | pubmed-2193543 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2002 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21935432008-04-14 Treatment with Soluble Interleukin-15Rα Exacerbates Intracellular Parasitic Infection by Blocking the Development of Memory CD8(+) T Cell Response Khan, Imtiaz A. Moretto, Magali Wei, Xiao-qing Williams, Martha Schwartzman, Joseph D. Liew, Foo Y. J Exp Med Article Interferon (IFN)-γ–producing CD8(+) T cells are important for the successful resolution of the obligate intracellular parasite Toxoplasma gondii by preventing the reactivation or controlling a repeat infection. Previous reports from our laboratory have shown that exogenous interleukin (IL)-15 treatment augments the CD8(+) T cell response against the parasite. However, the role of endogenous IL-15 in the proliferation of activated/memory CD8(+) T cells during toxoplasma or any other infection is unknown. In this study, we treated T. gondii immune mice with soluble IL-15 receptor α (sIL-15Rα) to block the host endogenous IL-15. The treatment markedly reduced the ability of the immune animals to control a lethal infection. CD8(+) T cell activities in the sIL-15Rα–administered mice were severely reduced as determined by IFN-γ release and target cell lysis assays. The loss of CD8(+) T cell immunity due to sIL-15Rα treatment was further demonstrated by adoptive transfer experiments. Naive recipients transferred with CD44(hi) activated/memory CD8(+) T cells and treated with sIL-15Rα failed to resist a lethal T. gondii infection. Moreover, sIL-15Rα treatment of the recipients blocked the ability of donor CD44(hi) activated/memory CD8(+) T cells to replicate in response to T. gondii challenge. To our knowledge, this is the first demonstration of the important role of host IL-15 in the development of antigen-specific memory CD8(+) T cells against an intracellular infection. The Rockefeller University Press 2002-06-03 /pmc/articles/PMC2193543/ /pubmed/12045244 http://dx.doi.org/10.1084/jem.20011915 Text en Copyright © 2002, 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 | Article Khan, Imtiaz A. Moretto, Magali Wei, Xiao-qing Williams, Martha Schwartzman, Joseph D. Liew, Foo Y. Treatment with Soluble Interleukin-15Rα Exacerbates Intracellular Parasitic Infection by Blocking the Development of Memory CD8(+) T Cell Response |
title | Treatment with Soluble Interleukin-15Rα Exacerbates Intracellular Parasitic Infection by Blocking the Development of Memory CD8(+) T Cell Response |
title_full | Treatment with Soluble Interleukin-15Rα Exacerbates Intracellular Parasitic Infection by Blocking the Development of Memory CD8(+) T Cell Response |
title_fullStr | Treatment with Soluble Interleukin-15Rα Exacerbates Intracellular Parasitic Infection by Blocking the Development of Memory CD8(+) T Cell Response |
title_full_unstemmed | Treatment with Soluble Interleukin-15Rα Exacerbates Intracellular Parasitic Infection by Blocking the Development of Memory CD8(+) T Cell Response |
title_short | Treatment with Soluble Interleukin-15Rα Exacerbates Intracellular Parasitic Infection by Blocking the Development of Memory CD8(+) T Cell Response |
title_sort | treatment with soluble interleukin-15rα exacerbates intracellular parasitic infection by blocking the development of memory cd8(+) t cell response |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193543/ https://www.ncbi.nlm.nih.gov/pubmed/12045244 http://dx.doi.org/10.1084/jem.20011915 |
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