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Tytuł pozycji:

CD73+ CD127high Long-Term Memory CD4 T Cells are Highly Proliferative in Response to Recall Antigens and Are Early Targets in HIV-1 Infection

Tytuł :
CD73+ CD127high Long-Term Memory CD4 T Cells are Highly Proliferative in Response to Recall Antigens and Are Early Targets in HIV-1 Infection
Autorzy :
Nabila Seddiki
John Zaunders
Chan Phetsouphanh
Vedran Brezar
Yin Xu
Helen M. McGuire
Michelle Bailey
Kristin McBride
Will Hey-Cunningham
Cynthia Mee Ling Munier
Laura Cook
Stephen Kent
Andrew Lloyd
Barbara Cameron
Barbara Fazekas de St Groth
Kersten Koelsch
Mark Danta
Hakim Hocini
Yves Levy
Anthony D. Kelleher
Pokaż więcej
Temat :
CD73
CD4+ subsets
HIV-1 viral reservoir
Biology (General)
QH301-705.5
Chemistry
QD1-999
Źródło :
International Journal of Molecular Sciences, Vol 22, Iss 912, p 912 (2021)
Wydawca :
MDPI AG, 2021.
Rok publikacji :
2021
Kolekcja :
LCC:Biology (General)
LCC:Chemistry
Typ dokumentu :
article
Opis pliku :
electronic resource
Język :
English
ISSN :
1422-0067
1661-6596
Relacje :
https://www.mdpi.com/1422-0067/22/2/912; https://doaj.org/toc/1661-6596; https://doaj.org/toc/1422-0067
DOI :
10.3390/ijms22020912
Dostęp URL :
https://doaj.org/article/f12f1736af7042aa8704d28c122403bb
Numer akcesji :
edsdoj.f12f1736af7042aa8704d28c122403bb
Czasopismo naukowe
HIV-1 infection rapidly leads to a loss of the proliferative response of memory CD4+ T lymphocytes, when cultured with recall antigens. We report here that CD73 expression defines a subset of resting memory CD4+ T cells in peripheral blood, which highly express the α-chain of the IL-7 receptor (CD127), but not CD38 or Ki-67, yet are highly proliferative in response to mitogen and recall antigens, and to IL-7, in vitro. These cells also preferentially express CCR5 and produce IL-2. We reasoned that CD73+ memory CD4+ T cells decrease very early in HIV-1 infection. Indeed, CD73+ memory CD4+ T cells comprised a median of 7.5% (interquartile range: 4.5–10.4%) of CD4+ T cells in peripheral blood from healthy adults, but were decreased in primary HIV-1 infection to a median of 3.7% (IQR: 2.6–6.4%; p = 0.002); and in chronic HIV-1 infection to 1.9% (IQR: 1.1–3%; p < 0.0001), and were not restored by antiretroviral therapy. Moreover, we found that a significant proportion of CD73+ memory CD4+ T cells were skewed to a gut-homing phenotype, expressing integrins α4 and β7, CXCR3, CCR6, CD161 and CD26. Accordingly, 20% of CD4+ T cells present in gut biopsies were CD73+. In HIV+ subjects, purified CD73+ resting memory CD4+ T cells in PBMC were infected with HIV-1 DNA, determined by real-time PCR, to the same level as for purified CD73-negative CD4+ T cells, both in untreated and treated subjects. Therefore, the proliferative CD73+ subset of memory CD4+ T cells is disproportionately reduced in HIV-1 infection, but, unexpectedly, their IL-7 dependent long-term resting phenotype suggests that residual infected cells in this subset may contribute significantly to the very long-lived HIV proviral DNA reservoir in treated subjects.
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