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HIV-Associated Microbial Translocation May Affect Cytokine Production of CD56bright NK Cells via Stimulation of Monocytes.

The Journal of infectious diseases

Authors: Michael ToVinh, Gregor Hörr, Christoph Hoffmeister, Kristiyana Dobrikova, Christina Gotter, Jan Raabe, Kim M Kaiser, Sarah Ahmad, Claudia Finnemann, Eyleen Matejec, Gudrun Hack, Jenny Bischoff, Gereon J Rieke, Carolynne Schwarze-Zander, Christoph Boesecke, Kathrin van Bremen, Jan-Christian Wasmuth, Anna M Eis-Hübinger, Hendrik Streeck, Hedda L Verhasselt, Johannes Oldenburg, Christian P Strassburg, Jürgen K Rockstroh, Ulrich Spengler, Benjamin Krämer, Jacob Nattermann

The mechanisms involved in HIV-associated natural killer (NK) cell impairment are still incompletely understood. We observed HIV infection to be associated with increased plasma levels of IFABP, a marker for gut epithelial barrier dysfunction, and LBP, a marker for microbial translocation. Both IFABP and LBP plasma concentrations were inversely correlated with NK cell interferon-γ production, suggesting microbial translocation to modulate NK cell functions. Accordingly, we found lipopolysaccharide to have an indirect inhibitory effect on NK cells via triggering monocytes' transforming growth factor-β production. Taken together, our data suggest increased microbial translocation to be involved in HIV-associated NK cell dysfunction.

© The Author(s) 2022. Published by Oxford University Press on behalf of Infectious Diseases Society of America. All rights reserved. For permissions, please e-mail:

PMID: 36520641

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