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http://hdl.handle.net/10451/18442
Título: | Comparison of the frequency of interleukin (IL)-2-, interferon-γ-, and IL-4-producing T cells in 2 diseases, human immunodeficiency virus types 1 and 2, with distinct clinical outcomes |
Autor: | Sousa, Ana E. Chaves, Ana F. Loureiro, Ana Victorino, Rui M. M. |
Data: | 2001 |
Editora: | Oxford University Press |
Citação: | The Journal of Infectious Diseases 2001;184:552–9 |
Resumo: | Human immunodeficiency virus (HIV) type 2 infection is associated with a better clinical outcome, slower rates of CD4 T cell decline, and lower viremia than is HIV-1. This study compares HIV-1 and HIV-2 in regard to the percentages of interleukin (IL)–2–, interferon (IFN)–γ–, and IL-4–producing cells at the single-cell level, as determined by flow cytometry. At a given degree of CD4 T cell depletion, the frequency of T cells able to produce IL-2 is better preserved in HIV-2 than in HIV-1 infection, particularly within the CD4 T cell subset. As described for HIV-1 immunodeficiency, HIV-2–positive patients exhibit a marked expansion of terminally differentiated effector CD8 T cells (CD28−CD27−IFN-γ+). However, the proportion of CD8 T cells able to simultaneously produce IL-2 and IFN-γ is higher in HIV-2 disease. Considering the central role of IL-2 as a lymphocyte proliferative and survival factor, these findings provide a possible immunologic basis for the distinct course of HIV-2 immunodeficiency |
Descrição: | © 2001 by the Infectious Diseases Society of America |
Peer review: | yes |
URI: | http://dx.doi.org/10.1086/322804 http://jid.oxfordjournals.org/content/184/5/552.long http://hdl.handle.net/10451/18442 |
ISSN: | 0022-1899 |
Versão do Editor: | The definitive version is available at http://www.oxfordjournals.org/ |
Aparece nas colecções: | FM-LIC - Artigos em Revistas Internacionais IMM - Artigos em Revistas Internacionais |
Ficheiros deste registo:
Ficheiro | Descrição | Tamanho | Formato | |
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Comparison_frequency.pdf | 195,79 kB | Adobe PDF | Ver/Abrir Acesso Restrito. Solicitar cópia ao autor! |
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