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HIV-associated microbial translocation may affect cytokine production of CD56bright NK cells via stimulation of monocytes.

Michael ToVinhGregor HörrChristoph HoffmeisterKristiyana DobrikovaChristina GotterJan RaabeKim M KaiserSarah AhmadClaudia FinnemannEyleen MatejecGudrun HackJenny BischoffGereon J RiekeCarolynne Schwarze-ZanderChristoph BoeseckeKathrin van BremenJan-Christian WasmuthAnna M Eis-HübingerHendrik StreeckHedda L VerhasseltJohannes OldenburgChristian P StrassburgJürgen K RockstrohUlrich SpenglerBenjamin KrämerJacob Nattermann
Published in: The Journal of infectious diseases (2022)
The mechanisms involved in HIV-associated 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 IFN-γ production, suggesting microbial translocation to modulate NK cell functions. Accordingly, we found LPS to have an indirect inhibitory effect on NK cells via triggering monocytes' TGF-β production. Taken together, our data suggest increased microbial translocation to be involved in HIV-associated NK cell dysfunction.
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