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Acquired resistance to Listeria monocytogenes is mediated by Lyt-2+ T cells independently of the influx of monocytes into granulomatous lesions
Facultative intracellular bacteria induce specific T cell responses of both the CD4+ and the CD8+ subsets. The immunohistological study of the tissue responses to Listeria monocytogenes in T cell subset-depleted, Listeria-primed mice revealed that CD4+ cells not only represent the predominant lympho...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1989
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2189398/ https://www.ncbi.nlm.nih.gov/pubmed/2502601 |
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collection | PubMed |
description | Facultative intracellular bacteria induce specific T cell responses of both the CD4+ and the CD8+ subsets. The immunohistological study of the tissue responses to Listeria monocytogenes in T cell subset-depleted, Listeria-primed mice revealed that CD4+ cells not only represent the predominant lymphocyte population in granulomatous lesions but mediate the attraction and accumulation of blood-borne monocytes into inflammatory foci. On the other hand, CD8+ T cells are able to mediate protection in the absence of CD4+ T cells, invading monocytes, and granulomatous inflammation, and therefore appear to activate resident macrophages for listericidal activity. |
format | Text |
id | pubmed-2189398 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1989 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21893982008-04-17 Acquired resistance to Listeria monocytogenes is mediated by Lyt-2+ T cells independently of the influx of monocytes into granulomatous lesions J Exp Med Articles Facultative intracellular bacteria induce specific T cell responses of both the CD4+ and the CD8+ subsets. The immunohistological study of the tissue responses to Listeria monocytogenes in T cell subset-depleted, Listeria-primed mice revealed that CD4+ cells not only represent the predominant lymphocyte population in granulomatous lesions but mediate the attraction and accumulation of blood-borne monocytes into inflammatory foci. On the other hand, CD8+ T cells are able to mediate protection in the absence of CD4+ T cells, invading monocytes, and granulomatous inflammation, and therefore appear to activate resident macrophages for listericidal activity. The Rockefeller University Press 1989-08-01 /pmc/articles/PMC2189398/ /pubmed/2502601 Text en 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 Acquired resistance to Listeria monocytogenes is mediated by Lyt-2+ T cells independently of the influx of monocytes into granulomatous lesions |
title | Acquired resistance to Listeria monocytogenes is mediated by Lyt-2+ T cells independently of the influx of monocytes into granulomatous lesions |
title_full | Acquired resistance to Listeria monocytogenes is mediated by Lyt-2+ T cells independently of the influx of monocytes into granulomatous lesions |
title_fullStr | Acquired resistance to Listeria monocytogenes is mediated by Lyt-2+ T cells independently of the influx of monocytes into granulomatous lesions |
title_full_unstemmed | Acquired resistance to Listeria monocytogenes is mediated by Lyt-2+ T cells independently of the influx of monocytes into granulomatous lesions |
title_short | Acquired resistance to Listeria monocytogenes is mediated by Lyt-2+ T cells independently of the influx of monocytes into granulomatous lesions |
title_sort | acquired resistance to listeria monocytogenes is mediated by lyt-2+ t cells independently of the influx of monocytes into granulomatous lesions |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2189398/ https://www.ncbi.nlm.nih.gov/pubmed/2502601 |