Innate Lymphoid Cells Are Depleted Irreversibly during Acute HIV-1 Infection in the Absence of Viral Suppression
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IMMUNITY-D-15-00665_R1 for Erja.pdf
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Author(s)
Kløverpris, Henrik N.
Mjösberg, Jenny
Mabuka, Jenniffer M.
Wellmann, Amanda
Ndhlovu, Zaza
Yadon, Marisa C.
Nhamoyebonde, Shepherd
Muenchhoff, Maximilian
Simoni, Yannick
Andersson, Frank
Alternative Title
Innate Lymphoid Cells Are Depleted Irreversibly during Acute HIV-1 Infection in the Absence of Viral Suppression
Date Issued
February 2016
Journal
Immunity
Publisher
Elsevier
Citation
Kløverpris, Henrik N. et al. “Innate Lymphoid Cells Are Depleted Irreversibly During Acute HIV-1 Infection in the Absence of Viral Suppression.” Immunity 44, 2 (February 2016): 391–405 © 2016 Elsevier Inc
Version
Original manuscript
Abstract
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. Keywords: innate lymphoid cells; HIV-1 infection
MIT Department
Institute for Medical Engineering and Science
Massachusetts Institute of Technology. Department of Chemistry
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Creative Commons Attribution-NonCommercial-NoDerivs License
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DOI of Published Version
https://doi.org/10.1016/j.immuni.2016.01.006
