Natural Killer Cells That Respond to Human Immunodeficiency Virus Type 1 (HIV-1) Peptides Are Associated with Control of HIV-1 Infection
Identifieur interne : 002661 ( Main/Exploration ); précédent : 002660; suivant : 002662Natural Killer Cells That Respond to Human Immunodeficiency Virus Type 1 (HIV-1) Peptides Are Associated with Control of HIV-1 Infection
Auteurs : Caroline T. Tiemessen [Afrique du Sud] ; Sharon Shalekoff [Afrique du Sud] ; Stephen Meddows-Taylor [Afrique du Sud] ; Diana B. Schramm [Afrique du Sud] ; Maria A. Papathanasopoulos [Afrique du Sud] ; Glenda E. Gray [Afrique du Sud] ; Gayle G. Sherman [Afrique du Sud] ; Ashraf H. Coovadia [Afrique du Sud] ; Louise Kuhn [États-Unis]Source :
- Journal of Infectious Diseases [ 0022-1899 ] ; 2010.
Abstract
Human immunodeficiency virus (HIV)-specific natural killer (CD3− cells) CD4, and CD8 T cellular responses were determined in 79 HIV-1-infected women in response to HIV-1 peptide pools (Gag, Pol, Nef, Reg, and Env) with use of a whole blood intracellular cytokine staining assay that measures interferon-γ and/or interleukin-2. HIV-specific CD3− cell responses to any region (Env and Reg predominantly targeted) were associated with lower viral load (P=.031) and higher CD4 T cell count (P=.015). Env-specific CD3− cell responses were stronger in women who had both Gag CD4 and CD8 T cell responses and, in turn, was associated with lower viral load (P=.005). CD3− cell responders had significantly higher representation of CD4 T cell responses to Env and Reg (P=.012 and P=.015, respectively) and higher magnitudes of CD4 T cell responses (P=.017 and P=.037, respectively) than did nonresponders. Peptide-specific natural killer cells are associated with markers of less severe disease progression among HIV-1-infected women (lower viral load and higher CD4 T cell count) and with stronger HIV-specific T cell responses.
Url:
DOI: 10.1086/656535
Affiliations:
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Sergievsky Centre, College of Physicians and Surgeons and Department of Epidemiology, Mailman School of Public Health, Columbia University, New York</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Infectious Diseases</title><title level="j" type="abbrev">J Infect Dis.</title><idno type="ISSN">0022-1899</idno><idno type="eISSN">1537-6613</idno><imprint><publisher>The University of Chicago Press</publisher><date type="published">2010</date><biblScope unit="vol">202</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1444">1444</biblScope><biblScope unit="page" to="1453">1453</biblScope></imprint><idno type="ISSN">0022-1899</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-1899</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Human immunodeficiency virus (HIV)-specific natural killer (CD3− cells) CD4, and CD8 T cellular responses were determined in 79 HIV-1-infected women in response to HIV-1 peptide pools (Gag, Pol, Nef, Reg, and Env) with use of a whole blood intracellular cytokine staining assay that measures interferon-γ and/or interleukin-2. HIV-specific CD3− cell responses to any region (Env and Reg predominantly targeted) were associated with lower viral load (P=.031) and higher CD4 T cell count (P=.015). Env-specific CD3− cell responses were stronger in women who had both Gag CD4 and CD8 T cell responses and, in turn, was associated with lower viral load (P=.005). CD3− cell responders had significantly higher representation of CD4 T cell responses to Env and Reg (P=.012 and P=.015, respectively) and higher magnitudes of CD4 T cell responses (P=.017 and P=.037, respectively) than did nonresponders. Peptide-specific natural killer cells are associated with markers of less severe disease progression among HIV-1-infected women (lower viral load and higher CD4 T cell count) and with stronger HIV-specific T cell responses.</div></front></TEI><affiliations><list><country><li>Afrique du Sud</li><li>États-Unis</li></country><region><li>Gauteng</li><li>État de New York</li></region><settlement><li>Johannesbourg</li></settlement><orgName><li>Université du Witwatersrand</li></orgName></list><tree><country name="Afrique du Sud"><noRegion><name sortKey="Tiemessen, Caroline T" sort="Tiemessen, Caroline T" uniqKey="Tiemessen C" first="Caroline T." last="Tiemessen">Caroline T. Tiemessen</name></noRegion><name sortKey="Coovadia, Ashraf H" sort="Coovadia, Ashraf H" uniqKey="Coovadia A" first="Ashraf H." last="Coovadia">Ashraf H. Coovadia</name><name sortKey="Gray, Glenda E" sort="Gray, Glenda E" uniqKey="Gray G" first="Glenda E." last="Gray">Glenda E. Gray</name><name sortKey="Meddows Taylor, Stephen" sort="Meddows Taylor, Stephen" uniqKey="Meddows Taylor S" first="Stephen" last="Meddows-Taylor">Stephen Meddows-Taylor</name><name sortKey="Papathanasopoulos, Maria A" sort="Papathanasopoulos, Maria A" uniqKey="Papathanasopoulos M" first="Maria A." last="Papathanasopoulos">Maria A. Papathanasopoulos</name><name sortKey="Schramm, Diana B" sort="Schramm, Diana B" uniqKey="Schramm D" first="Diana B." last="Schramm">Diana B. Schramm</name><name sortKey="Shalekoff, Sharon" sort="Shalekoff, Sharon" uniqKey="Shalekoff S" first="Sharon" last="Shalekoff">Sharon Shalekoff</name><name sortKey="Sherman, Gayle G" sort="Sherman, Gayle G" uniqKey="Sherman G" first="Gayle G." last="Sherman">Gayle G. Sherman</name><name sortKey="Sherman, Gayle G" sort="Sherman, Gayle G" uniqKey="Sherman G" first="Gayle G." last="Sherman">Gayle G. Sherman</name><name sortKey="Tiemessen, Caroline T" sort="Tiemessen, Caroline T" uniqKey="Tiemessen C" first="Caroline T." last="Tiemessen">Caroline T. Tiemessen</name><name sortKey="Tiemessen, Caroline T" sort="Tiemessen, Caroline T" uniqKey="Tiemessen C" first="Caroline T." last="Tiemessen">Caroline T. Tiemessen</name></country><country name="États-Unis"><region name="État de New York"><name sortKey="Kuhn, Louise" sort="Kuhn, Louise" uniqKey="Kuhn L" first="Louise" last="Kuhn">Louise Kuhn</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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