Journal
IMMUNITY
Volume 44, Issue 2, Pages 391-405Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2016.01.006
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Funding
- Danish Agency for Science, Technology and Innovation [12-132295]
- Lundbeck Foundation [R151-2013-14624]
- MAERSK Foundation
- Collaboration for AIDS Vaccine Discovery of the Bill and Melinda Gates Foundation
- NIH [AI067073]
- Bill and Melinda Gates Foundation
- International AIDS Vaccine Initiative (IAVI) [UKZNRSA1001]
- NIAID [R37AI067073]
- International Early Career Scientist Award from the Howard Hughes Medical Institute
- Victor Daitz Foundation
- National Science Foundation Graduate Research Fellowship Program (NSF GRFP)
- Searle Scholars Program
- South African Research Chairs Initiative
- Lundbeck Foundation [R151-2013-14624] Funding Source: researchfish
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Innate lymphoid cells (ILCs) play a central role in the response to infection by secreting cytokines crucial for immune regulation, tissue homeostasis, and repair. Although dysregulation of these systems is central to pathology, the impact of HIV-1 on ILCs remains unknown. We found that human blood ILCs were severely depleted during acute viremic HIV-1 infection and that ILC numbers did not recover after resolution of peak viremia. ILC numbers were preserved by antiretroviral therapy (ART), but only if initiated during acute infection. Transcriptional profiling during the acute phase revealed upregulation of genes associated with cell death, temporally linked with a strong IFN acute-phase response and evidence of gut barrier breakdown. We found no evidence of tissue redistribution in chronic disease and remaining circulating ILCs were activated but not apoptotic. These data provide a potential mechanistic link between acute HIV-1 infection, lymphoid tissue breakdown, and persistent immune dysfunction.
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