HIV-1 infection of macrophages differentially primes NK-cell cytotoxicity and proinflammatory cytokine production

Summary: Natural killer (NK) cells are innate cytotoxic lymphocytes with antiviral functions explored in “shock and kill” strategies to eliminate the HIV-1 reservoir. For optimal activity against infected targets, NK cells require priming. This study examined how macrophages prime NK cells following...

Full description

Saved in:
Bibliographic Details
Main Authors: Leonore Mensching, Maya Beiersdorfer, Sebastian Schloer, Sandra Köllmann, Friederike Reinsberg, Benedetta Padoan, Pia Fittje, Timo Trenkner, Annika Zaayenga, Gloria Martrus, Maher Almahfoud, Christina M. Stürzel, Daniel Sauter, Frank Kirchhoff, Julian Schulze zur Wiesch, Marcus Altfeld, Wilfredo F. Garcia-Beltran, Angelique Hoelzemer
Format: Article
Language:English
Published: Elsevier 2025-07-01
Series:iScience
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S258900422501140X
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850121817341034496
author Leonore Mensching
Maya Beiersdorfer
Sebastian Schloer
Sandra Köllmann
Friederike Reinsberg
Benedetta Padoan
Pia Fittje
Timo Trenkner
Annika Zaayenga
Gloria Martrus
Maher Almahfoud
Christina M. Stürzel
Daniel Sauter
Frank Kirchhoff
Julian Schulze zur Wiesch
Marcus Altfeld
Wilfredo F. Garcia-Beltran
Angelique Hoelzemer
author_facet Leonore Mensching
Maya Beiersdorfer
Sebastian Schloer
Sandra Köllmann
Friederike Reinsberg
Benedetta Padoan
Pia Fittje
Timo Trenkner
Annika Zaayenga
Gloria Martrus
Maher Almahfoud
Christina M. Stürzel
Daniel Sauter
Frank Kirchhoff
Julian Schulze zur Wiesch
Marcus Altfeld
Wilfredo F. Garcia-Beltran
Angelique Hoelzemer
author_sort Leonore Mensching
collection DOAJ
description Summary: Natural killer (NK) cells are innate cytotoxic lymphocytes with antiviral functions explored in “shock and kill” strategies to eliminate the HIV-1 reservoir. For optimal activity against infected targets, NK cells require priming. This study examined how macrophages prime NK cells following HIV-1 infection. We found that HIV-1-infected monocyte-derived macrophages upregulated membrane-bound IL-15Rα, NKG2D ligands, CD48, and IL-18. While crosstalk between NK cells and infected macrophages enhanced proinflammatory cytokine production, it led to only weak priming of NK-cell cytotoxicity. In people living with HIV-1 (PLWH) on antiretroviral therapy, macrophage priming remained intact and polyfunctional, with the strongest response in CD56dim KIR+ and/or NKG2A+ NK cells. However, CD56neg NK cells —a subset unique to HIV-1 infection— remained dysfunctional. These findings elucidate how HIV-1 alters macrophage-NK cell crosstalk and underscore the need for therapeutic strategies that enhance NK-cell cytotoxicity in efforts toward a functional HIV-1 cure.
format Article
id doaj-art-3dae15ae49ca4d0e87de972d9e1f6826
institution OA Journals
issn 2589-0042
language English
publishDate 2025-07-01
publisher Elsevier
record_format Article
series iScience
spelling doaj-art-3dae15ae49ca4d0e87de972d9e1f68262025-08-20T02:35:00ZengElsevieriScience2589-00422025-07-0128711287910.1016/j.isci.2025.112879HIV-1 infection of macrophages differentially primes NK-cell cytotoxicity and proinflammatory cytokine productionLeonore Mensching0Maya Beiersdorfer1Sebastian Schloer2Sandra Köllmann3Friederike Reinsberg4Benedetta Padoan5Pia Fittje6Timo Trenkner7Annika Zaayenga8Gloria Martrus9Maher Almahfoud10Christina M. Stürzel11Daniel Sauter12Frank Kirchhoff13Julian Schulze zur Wiesch14Marcus Altfeld15Wilfredo F. Garcia-Beltran16Angelique Hoelzemer17Department of Medicine, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany; Research Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, GermanyDepartment of Medicine, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, GermanyInstitute of Immunology, Research Group Immunopharmacology, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, GermanyDepartment of Medicine, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany; Research Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, GermanyDepartment of Medicine, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany; Research Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, Germany; German Center for Infection Research (DZIF), Site Hamburg-Lübeck-Borstel-Riems, Borstel, GermanyResearch Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, GermanyResearch Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, GermanyDepartment of Medicine, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, GermanyDepartment of Medicine, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, GermanyResearch Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, GermanyDepartment of Medicine, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, GermanyInstitute of Molecular Virology, University Medical Center, Ulm, GermanyInstitute for Medical Virology and Epidemiology of Viral Diseases, Eberhard Karls University Tübingen, Tübingen, GermanyInstitute of Molecular Virology, University Medical Center, Ulm, GermanyDepartment of Medicine, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany; German Center for Infection Research (DZIF), Site Hamburg-Lübeck-Borstel-Riems, Borstel, GermanyResearch Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, GermanyRagon Institute of Massachusetts General Hospital, MIT and Harvard, Cambridge, MA, USA; Department of Pathology, Massachusetts General Hospital/Harvard Medical School, Boston, MA, USADepartment of Medicine, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany; Research Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, Germany; German Center for Infection Research (DZIF), Site Hamburg-Lübeck-Borstel-Riems, Borstel, Germany; Institute for Infection and Vaccine Development (IIRVD), University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany; Corresponding authorSummary: Natural killer (NK) cells are innate cytotoxic lymphocytes with antiviral functions explored in “shock and kill” strategies to eliminate the HIV-1 reservoir. For optimal activity against infected targets, NK cells require priming. This study examined how macrophages prime NK cells following HIV-1 infection. We found that HIV-1-infected monocyte-derived macrophages upregulated membrane-bound IL-15Rα, NKG2D ligands, CD48, and IL-18. While crosstalk between NK cells and infected macrophages enhanced proinflammatory cytokine production, it led to only weak priming of NK-cell cytotoxicity. In people living with HIV-1 (PLWH) on antiretroviral therapy, macrophage priming remained intact and polyfunctional, with the strongest response in CD56dim KIR+ and/or NKG2A+ NK cells. However, CD56neg NK cells —a subset unique to HIV-1 infection— remained dysfunctional. These findings elucidate how HIV-1 alters macrophage-NK cell crosstalk and underscore the need for therapeutic strategies that enhance NK-cell cytotoxicity in efforts toward a functional HIV-1 cure.http://www.sciencedirect.com/science/article/pii/S258900422501140XImmunologyImmune responseVirology
spellingShingle Leonore Mensching
Maya Beiersdorfer
Sebastian Schloer
Sandra Köllmann
Friederike Reinsberg
Benedetta Padoan
Pia Fittje
Timo Trenkner
Annika Zaayenga
Gloria Martrus
Maher Almahfoud
Christina M. Stürzel
Daniel Sauter
Frank Kirchhoff
Julian Schulze zur Wiesch
Marcus Altfeld
Wilfredo F. Garcia-Beltran
Angelique Hoelzemer
HIV-1 infection of macrophages differentially primes NK-cell cytotoxicity and proinflammatory cytokine production
iScience
Immunology
Immune response
Virology
title HIV-1 infection of macrophages differentially primes NK-cell cytotoxicity and proinflammatory cytokine production
title_full HIV-1 infection of macrophages differentially primes NK-cell cytotoxicity and proinflammatory cytokine production
title_fullStr HIV-1 infection of macrophages differentially primes NK-cell cytotoxicity and proinflammatory cytokine production
title_full_unstemmed HIV-1 infection of macrophages differentially primes NK-cell cytotoxicity and proinflammatory cytokine production
title_short HIV-1 infection of macrophages differentially primes NK-cell cytotoxicity and proinflammatory cytokine production
title_sort hiv 1 infection of macrophages differentially primes nk cell cytotoxicity and proinflammatory cytokine production
topic Immunology
Immune response
Virology
url http://www.sciencedirect.com/science/article/pii/S258900422501140X
work_keys_str_mv AT leonoremensching hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT mayabeiersdorfer hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT sebastianschloer hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT sandrakollmann hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT friederikereinsberg hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT benedettapadoan hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT piafittje hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT timotrenkner hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT annikazaayenga hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT gloriamartrus hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT maheralmahfoud hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT christinamsturzel hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT danielsauter hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT frankkirchhoff hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT julianschulzezurwiesch hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT marcusaltfeld hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT wilfredofgarciabeltran hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction
AT angeliquehoelzemer hiv1infectionofmacrophagesdifferentiallyprimesnkcellcytotoxicityandproinflammatorycytokineproduction