학술논문
Mitochondrial Dysfunction Contributes to Impaired Cytokine Production of CD56bright Natural Killer Cells From Human Immunodeficiency Virus-Infected Individuals Under Effective Antiretroviral Therapy.
Document Type
Journal Article
Author
ToVinh, Michael; Hörr, Gregor; Dobrikova, Kristiyana; Gotter, Christina; Rommel, Clemens; Hoffmeister, Christoph; Raabe, Jan; Kaiser, Kim M; Finnemann, Claudia; Bischoff, Jenny; Rieke, Gereon J; Wilhelm, Christoph; Schmitt, Vanessa; Möhl, Christoph; Aghabeig, Mansoureh; Schwarze-Zander, Carolynne; Boesecke, Christoph; Bremen, Kathrin van; Wasmuth, Jan Christian; Strassburg, Christian P
Source
Subject
*HIV infection complications
*CYTOKINES
*KILLER cells
*MITOCHONDRIA
*RESEARCH funding
*HIV
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Language
ISSN
0022-1899
Abstract
Human immunodeficiency virus (HIV) infection is associated with impaired natural killer (NK) cell activity, which is only incompletely restored under antiretroviral therapy. Analyzing the bioenergetics profiles of oxygen consumption, we observed that several parameters were significantly reduced in HIV+ NK cells, indicating a mitochondrial defect. Accordingly, we found HIV+ CD56bright NK cells to display a decreased mitochondrial membrane potential and mitochondrial mass. Both parameters were positively correlated with interferon gamma (IFN-γ) production of NK cells. Finally, we demonstrated that stimulation of HIV+ NK cells with MitoTEMPO, a mitochondria-targeting antioxidant, significantly improved IFN-γ production. We identified mitochondrial dysfunction as a mechanism that contributes to impaired NK cell function. [ABSTRACT FROM AUTHOR]