Loss of CCR7 Expression on CD56bright NK Cells Is Associated with a CD56dimCD16+ NK Cell-Like Phenotype and Correlates with HIV Viral Load |
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Authors: | Henoch S. Hong Fareed Ahmad Johanna M. Eberhard Nupur Bhatnagar Benjamin A. Bollmann Phillip Keudel Matthias Ballmaier Margot Zielinska-Skowronek Reinhold E. Schmidt Dirk Meyer-Olson |
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Affiliation: | 1. Klinik für Immunologie und Rheumatologie, Medizinische Hochschule Hannover, Hannover, Germany.; 2. Division of Immunology, New England Primate Research Center, Harvard Medical School, Southborough, Massachusetts, United States of America.; 3. Pädiatrische Hämatologie und Onkologie, Medizinische Hochschule Hannover, Hannover, Germany.; University of Sydney, Australia, |
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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 CD56dimCD16+ and CD56−CD16+ NK cells. However, the impact of HIV-infection on CD56bright NK cells is less well understood. Here we report a rise of CD56bright NK cells in HIV-infected individuals, which lack CCR7-expression and strongly correlate with HIV viral load. CCR7−CD56bright 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 CD56dimCD16+ NK cells. Furthermore, CD56bright 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 CD56bright NK cells, which provides a novel aspect of HIV-associated pathogenesis within the NK cell compartment. |
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