Dynamic MAIT cell response with progressively enhanced innateness during acute HIV-1 infection.
Biomarkers
/ blood
C-Reactive Protein
/ metabolism
Cohort Studies
HIV Infections
/ immunology
HIV-1
/ physiology
Humans
Immunity, Innate
/ genetics
Interferon Regulatory Factors
/ genetics
Lipopolysaccharide Receptors
/ metabolism
Lymphocyte Activation
Mucosal-Associated Invariant T Cells
/ immunology
Receptors, Antigen, T-Cell
/ genetics
Transcriptome
Viremia
/ immunology
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
14 01 2020
14 01 2020
Historique:
received:
14
03
2019
accepted:
10
12
2019
entrez:
16
1
2020
pubmed:
16
1
2020
medline:
24
4
2020
Statut:
epublish
Résumé
Mucosa-associated invariant T (MAIT) cell loss in chronic HIV-1 infection is a significant insult to antimicrobial immune defenses. Here we investigate the response of MAIT cells during acute HIV-1 infection utilizing the RV217 cohort with paired longitudinal pre- and post-infection samples. MAIT cells are activated and expand in blood and mucosa coincident with peak HIV-1 viremia, in a manner associated with emerging microbial translocation. This is followed by a phase with elevated function as viral replication is controlled to a set-point level, and later by their functional decline at the onset of chronic infection. Interestingly, enhanced innate-like pathways and characteristics develop progressively in MAIT cells during infection, in parallel with TCR repertoire alterations. These findings delineate the dynamic MAIT cell response to acute HIV-1 infection, and show how the MAIT compartment initially responds and expands with enhanced function, followed by progressive reprogramming away from TCR-dependent antibacterial responses towards innate-like functionality.
Identifiants
pubmed: 31937782
doi: 10.1038/s41467-019-13975-9
pii: 10.1038/s41467-019-13975-9
pmc: PMC6959336
doi:
Substances chimiques
Biomarkers
0
CD14 protein, human
0
Interferon Regulatory Factors
0
Lipopolysaccharide Receptors
0
Receptors, Antigen, T-Cell
0
interferon regulatory factor-4
0
C-Reactive Protein
9007-41-4
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
272Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK108350
Pays : United States
Organisme : U.S. Department of Defense (United States Department of Defense)
ID : W81XWH-07-2-0067
Pays : International
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