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CD73+ CD127high long-term memory CD4 T cells are highly proliferative in response to recall antigens and are early targets in HIV-1 infection

ABSTRACT: CD73+ CD127high long-term memory CD4 T cells are highly proliferative in response to recall antigens and are early targets in HIV-1 infection

PROVIDER: PRJNA674574 | ENA |

REPOSITORIES: ENA

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CD73+ CD127high long-term memory CD4 T cells are highly proliferative in response to recall antigens and are early targets in HIV-1 infection

Project description: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 which highly express the alpha-chain of the receptor for IL-7 (CD127), but not CD38 or Ki-67 in vivo, 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 early in HIV-1 infection. We compared gene expression profiles of healthy subjects recovered CD4+CD73+ to CD4+CD73- T cells, and also CD8+CD73+ to CD8+CD73- T cells

2021-02-02 | GSE160805 | GEO

CD73<sup>+</sup> CD127<sup>high</sup> Long-Term Memory CD4 T Cells Are Highly Proliferative in Response to Recall Antigens and Are Early Targets in HIV-1 Infection.

Project description: Not available

| S-EPMC7831934 | biostudies-literature

The Hypoxia-regulated Ectonucleotidase CD73 is a Host Determinant of HIV Latency [Array]

Project description:Deciphering the mechanisms underlying viral persistence is critical to achieving a cure for HIV infection. Here, we implement a systems approach to discover molecular signatures of HIV latently-infected CD4+ T cells, identifying the immunosuppressive, adenosine-producing ectonucleotidase CD73 as a key surface marker of latent cells. Hypoxic conditioning, reflecting the lymphoid tissue microenvironment, increases the frequency of CD73+ CD4+ T cells and promotes HIV latency. Transcriptomic profiles of CD73+ CD4+ T cells favor viral quiescence, immune evasion, and cell survival. CD73+ CD4+ T cells are capable of harboring a functional HIV reservoir and reinitiating productive infection ex vivo. CD73 or adenosine receptor blockade facilitates latent HIV reactivation in vitro, mechanistically linking adenosine signaling to viral quiescence. Finally, tissue imaging of lymph nodes from HIV-infected individuals on antiretroviral therapy reveals spatial association between CD73 expression and HIV persistence in vivo. Our findings warrant development of HIV cure strategies targeting the hypoxia-CD73-adenosine axis.

2023-09-24 | GSE243577 | GEO

The Hypoxia-regulated Ectonucleotidase CD73 is a Host Determinant of HIV Latency [RNA-seq]

2023-09-28 | GSE244190 | GEO

CD73+ memory CD4 T cells are a long-lived population with elevated effector function and prone to differentiate into TRM-like cells [ATAC-seq]

Project description:The understanding of heterogeneity of human memory T cells will help to know the function, development and maintenance of memory population, then to improve the recall response or effective immunotherapy. Ecto-5’-nucleotidase CD73 expression in four subsets of memory T cells decreases with aging. The resistance to apoptosis and high expression of IL7R entitle CD73+ memory T cells to be long-lived population. We found antigen-specific memory T cells have overwhelming CD73 expression. The transcriptional and chromatin accessibility profiles indicate the elevated effector functions in CD73+ memory CD4 T cells comparing to CD73- counterparts. Homer analysis and Transcriptional factor (TF)-regulatory element-target gene triplet network clearly show the crucial role of RUNT and NR family TFs in CD73+ cells. Furthermore, CD73+ memory CD4 T cells were prone to differentiate into TRM-like cells under in-vitro sequential TCR and TGF/IL-15 signaling. The decreased percentage of CD73+ memory T cells with age leads to the less replenishment of TRM cells from peripheral blood.

2021-08-28 | GSE157162 | GEO

CD73+ memory CD4 T cells are a long-lived population with elevated effector function and prone to differentiate into TRM-like cells [RNA-seq]

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Expression data from CD73 positive adipose derived mesenchymal stem cells (CD73+ AD-MSCs) and CD73 negative adipose derived mesenchymal stem cells (CD73- AD-MSCs) of mouse

Project description:MSCs are a heterogeneous population and the specific population of MSCs may exhibit a selective ability for tissue repair. The aim of our research was to adapt the CD73+ subgroup of adipose derived MSCs (AD-MSCs) for the therapy of myocardial infarction (MI). Our results revealed that CD73+ AD-MSCs played more effective role in the acceleration function of cardiac recovery by promoting angiogenesis in a rat model of MI compared to mixed AD-MSCs and CD73- AD-MSCs. Microarray analysis shows differences between CD73+ and CD73- AD-MSCs when transcription profile of these two subgroups were compared, especially in VEGF pathway.

2021-06-02 | GSE167219 | GEO

Pneumococcal conjugate vaccination at birth induces robust recall responses at 9 months of age.

Project description:The objective of this study was to compare recall responses to vaccine antigens at 3 months and 9 months of age in infants who were vaccinated at birth or at 1 month.

2011-06-27 | GSE25263 | GEO

Pneumococcal conjugate vaccination at birth induces robust recall responses at 9 months of age.

Project description:The objective of this study was to compare recall responses to vaccine antigens at 3 months and 9 months of age in infants who were vaccinated at birth or at 1 month. PBMC were obtained at 9 months of age from infants who were vaccinated at birth (n=25) or 1 month (n=25). The PBMC were cultured in the presence or absence of CRM197 antigen for 72 hours. At the termination of the cultures, total RNA was extracted from the PBMC. The RNA was pooled into groups of n=5 subjects per group, following by labeling and hybridization to Affymetrix microarrays.

2011-06-27 | E-GEOD-25263 | biostudies-arrayexpress

CD73 knockdown effect in pancreatic cancer cell lines

Project description:Recent studies have shown that non-enzymatic function of CD73 play a key role in tumor progression, but this function of CD73 in pancreatic cancer cells has not been studied. In the present study, PANC-1 cell lines were transfected with CD73 siRNA, and proliferation ability and cell cycle was significantly inhibited. However, little is known about the mechanisms involved in CD73 regulation in tumors.

2018-07-13 | GSE117012 | GEO

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