| Autor: |
Kaufmann, Daniel E, Kavanagh, Daniel G, Pereyra, Florencia, Zaunders, John J, Mackey, Elizabeth W, Miura, Toshiyuki, Palmer, Sarah, Brockman, Mark, Rathod, Almas, Piechocka-Trocha, Alicja, Baker, Brett, Zhu, Baogong, Le Gall, Sylvie, Waring, Michael T, Ahern, Ryan, Moss, Kristin, Kelleher, Anthony D, Coffin, John M, Freeman, Gordon J, Rosenberg, Eric S |
| Zdroj: |
Nature Immunology; Nov2007, Vol. 8 Issue 11, p1246-1254, 9p, 5 Graphs |
| Abstrakt: |
In progressive viral infection, antiviral T cell function is impaired by poorly understood mechanisms. Here we report that the inhibitory immunoregulatory receptor CTLA-4 was selectively upregulated in human immunodeficiency virus (HIV)–specific CD4+ T cells but not CD8+ T cells in all categories of HIV-infected subjects evaluated, with the exception of rare people able to control viremia in the absence of antiretroviral therapy. CTLA-4 expression correlated positively with disease progression and negatively with the capacity of CD4+ T cells to produce interleukin 2 in response to viral antigen. Most HIV-specific CD4+ T cells coexpressed CTLA-4 and another inhibitory immunoregulatory receptor, PD-1. In vitro blockade of CTLA-4 augmented HIV-specific CD4+ T cell function. These data, indicating a reversible immunoregulatory pathway selectively associated with CD4+ T cell dysfunction, provide a potential target for immunotherapy in HIV-infected patients. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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