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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE157163 | GEO | 2021/08/28

REPOSITORIES: GEO

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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 Immune Checkpoint Defines Inducible Regulatory NK cells in the Tumor Microenvironment

Project description:High levels of ecto-5'-nucleotidase (CD73) have been implicated in immune suppression and tumor progression. Elevated levels of CD73 has also been observed in patients who progress on anti–PD-1 immunotherapy. While regulatory T cells can express CD73 and inhibit T cell responses via the production of adenosine, less is known if conventional T cells and natural killer (NK) cells can express CD73. We found that the expression of CD73 is restricted to tumor-infiltrating NK cells and the frequency of these cells correlate with larger tumor size in patients with breast cancer. In addition, the expression of other immune checkpoint receptors including LAG-3 and VISTA was significantly higher in CD73 positive NK cells than on CD73 negative NK cells. Furthermore, the prognostic value of CD73 gene expression was influenced by NK cell signature expressed in patients with breast cancer and sarcoma. Mechanistically, upon engagement of 4-1BBL on tumor cells, NK cells transport CD73 in intracellular vesicles to the cell surface and extracellular space via actin polymerization-dependent exocytosis. These CD73 positive NK cells undergo transcriptional reprogramming and upregulate IL10 production via STAT3 transcriptional activity and suppress CD4 T cell activity. Altogether, our results support that tumors can hijack NK cells as a means to escape immunity and that CD73 expression defines an inducible population of NK cells with immune regulatory properties within the tumor microenvironment.

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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

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Effector TH17 cells give rise to long-lived TRM cells that are essential for an immediate response against bacterial infection

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Effector TH17 cells give rise to long-lived TRM cells that are essential for an immediate response against bacterial infection

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

Project description:CD73+ memory CD4 T cells are a long-lived population with elevated effector function and prone to differentiate into TRM-like cells

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

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