Abstract
NK cells are pivotal sentinels of the innate immune system and distinct subpopulations in peripheral blood have been described. A number of studies addressed HIV-induced alterations of NK cell phenotype and functionality mainly focusing on CD56(dim)CD16⁺ and CD56⁻CD16⁺ NK cells. However, the impact of HIV-infection on CD56(bright) NK cells is less well understood. Here we report a rise of CD56(bright) NK cells in HIV-infected individuals, which lack CCR7-expression and strongly correlate with HIV viral load. CCR7⁻CD56(bright) NK cells were characterized by increased cytolytic potential, higher activation states and a more differentiated phenotype. These cells thus acquired a number of features of CD56(dim)CD16⁺ NK cells. Furthermore, CD56(bright) NK cells from HIV patients exhibited higher degranulation levels compared to uninfected individuals. Thus, chronic HIV-infection is associated with a phenotypic and functional shift of CD56(bright) NK cells, which provides a novel aspect of HIV-associated pathogenesis within the NK cell compartment.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adult
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Apoptosis
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Biomarkers / metabolism
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CD56 Antigen / metabolism*
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Female
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Gene Expression Regulation*
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HIV-1 / physiology*
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Humans
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Killer Cells, Natural / cytology
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Killer Cells, Natural / metabolism
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Killer Cells, Natural / virology*
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Male
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Phenotype
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Receptors, CCR7 / deficiency
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Receptors, CCR7 / metabolism*
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Receptors, IgG / metabolism*
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Viral Load*
Substances
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Biomarkers
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CCR7 protein, human
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CD56 Antigen
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Receptors, CCR7
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Receptors, IgG
Grants and funding
D.M.O. is supported by grants from the Bundesministerium für Bildung und Forschung, Stiftung Zukunfts- und Innovationsfonds Niedersachsen, the European AIDS Treatment Network (NEAT) and the Helmholtz-Zentrum für Infektionsforschung (IG-SCID-TwinPro02). H.S.H. is supported by a fellowship from the MD/PhD program of the Hannover Biomedical Research School (HBRS) at Hannover Medical School and by a post-doctoral fellowship from the Deutsche Forschungsgemeinschaft (HO 4527/1-1). R.E.S. is supported by grant IND 06/20 from Bundesministerium für Bildung und Forschung and NEAT. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.