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Tytuł pozycji:

Infection-induced type I interferons critically modulate the homeostasis and function of CD8 + naïve T cells.

Tytuł:
Infection-induced type I interferons critically modulate the homeostasis and function of CD8 naïve T cells.
Autorzy:
Jergović M; Department of Immunobiology and the University of Arizona Center on Aging, University of Arizona College of Medicine, Tucson, AZ, USA.
Coplen CP; Department of Immunobiology and the University of Arizona Center on Aging, University of Arizona College of Medicine, Tucson, AZ, USA.
Uhrlaub JL; Department of Immunobiology and the University of Arizona Center on Aging, University of Arizona College of Medicine, Tucson, AZ, USA.
Besselsen DG; University Animal Care, University of Arizona, Tucson, AZ, USA.
Cheng S; Department of Medicine, University of Arizona College of Medicine, Tucson, AZ, USA.
Smithey MJ; Department of Immunobiology and the University of Arizona Center on Aging, University of Arizona College of Medicine, Tucson, AZ, USA.; Vir, Inc., San Francisco, CA, USA.
Nikolich-Žugich J; Department of Immunobiology and the University of Arizona Center on Aging, University of Arizona College of Medicine, Tucson, AZ, USA. .
Źródło:
Nature communications [Nat Commun] 2021 Sep 06; Vol. 12 (1), pp. 5303. Date of Electronic Publication: 2021 Sep 06.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Original Publication: [London] : Nature Pub. Group
MeSH Terms:
Antigens, Ly/*genetics
CD8-Positive T-Lymphocytes/*immunology
Homeostasis/*genetics
Immunologic Memory/*genetics
Interferon-alpha/*genetics
Interferon-gamma/*genetics
West Nile Fever/*genetics
Animals ; Antigens, Ly/immunology ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/virology ; CD5 Antigens/genetics ; CD5 Antigens/immunology ; CD8 Antigens/genetics ; CD8 Antigens/immunology ; CD8-Positive T-Lymphocytes/virology ; Cell Differentiation ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Homeostasis/immunology ; Interferon-alpha/immunology ; Interferon-gamma/immunology ; Interleukin-7/genetics ; Interleukin-7/immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, T-Cell/genetics ; Receptors, Antigen, T-Cell/immunology ; Signal Transduction ; West Nile Fever/immunology ; West Nile Fever/pathology ; West Nile Fever/virology ; West Nile virus/immunology ; West Nile virus/pathogenicity
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Grant Information:
R01 AG020719 United States AG NIA NIH HHS; R01 AG048021 United States AG NIA NIH HHS; R37 AG020719 United States AG NIA NIH HHS
Substance Nomenclature:
0 (Antigens, Ly)
0 (CD5 Antigens)
0 (CD8 Antigens)
0 (Cd5 protein, mouse)
0 (Interferon-alpha)
0 (Interleukin-7)
0 (Ly-6C antigen, mouse)
0 (Receptors, Antigen, T-Cell)
82115-62-6 (Interferon-gamma)
Entry Date(s):
Date Created: 20210907 Date Completed: 20211005 Latest Revision: 20240114
Update Code:
20240114
PubMed Central ID:
PMC8421345
DOI:
10.1038/s41467-021-25645-w
PMID:
34489451
Czasopismo naukowe
Naïve T (Tn) cells require two homeostatic signals for long-term survival: tonic T cell receptor:self-peptide-MHC contact and IL-7 stimulation. However, how microbial exposure impacts Tn homeostasis is still unclear. Here we show that infections can lead to the expansion of a subpopulation of long-lived, Ly6C + CD8 + Tn cells with accelerated effector function. Mechanistically, mono-infection with West Nile virus transiently, and polymicrobial exposure persistently, enhances Ly6C expression selectively on CD5 hi CD8 + cells, which in the case of polyinfection translates into a numerical CD8 + Tn cell increase in the lymph nodes. This conversion and expansion of Ly6C + Tn cells depends on IFN-I, which upregulates MHC class I expression and enhances tonic TCR signaling in differentiating Tn cells. Moreover, for Ly6C + CD8 +  Tn cells, IFN-I-mediated signals optimize their homing to secondary sites, extend their lifespan, and enhance their effector differentiation and antibacterial function, particularly for low-affinity clones. Our results thus uncover significant regulation of Tn homeostasis and function via infection-driven IFN-I, with potential implications for immunotherapy.
(© 2021. The Author(s).)
Erratum in: Nat Commun. 2024 Jan 11;15(1):470. (PMID: 38212327)

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