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Myeloid cell subsets that express latency-associated peptide promote cancer growth by modulating T cells

ABSTRACT: Myeloid cell subsets that express latency-associated peptide promote cancer growth by modulating T cells

PROVIDER: PRJNA728109 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14466778_1.fastq.gz	Fastqsanger.gz
	SRR14466778_2.fastq.gz	Fastqsanger.gz
	SRR14466779_1.fastq.gz	Fastqsanger.gz
	SRR14466779_2.fastq.gz	Fastqsanger.gz
	SRR14466780_1.fastq.gz	Fastqsanger.gz

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Myeloid cell subsets that express latency-associated peptide promote cancer growth by modulating T cells

Project description:Myeloid suppressor cells promote tumor growth by a variety of mechanisms which are not fully characterized. We identified myeloid cells (MCs) expressing the latency-associated peptide (LAP) of TGF-b on their surface, LAPHi MCs, that stimulate Foxp3+ Tregs while inhibiting effector T cell proliferation and function. Blocking TGF-b inhibits the tolerogenic ability of LAPHi MCs. Furthermore, adoptive transfer of LAPHi MCs promote Treg accumulation and tumor growth in vivo. Conversely, anti-LAP antibody, which reduces LAPHi MCs, slows cancer progression. Single-cell RNA-Seq analysis on tumor-derived immune cells revealed LAPHi dominated cell subsets with distinct immunosuppressive signatures, including those with high levels of MHCII and PD-L1 genes. Analogous to mice, LAP is expressed on myeloid suppressor cells in humans, and these cells are increased in glioma patients. Thus, our results identify a previously unknown function by which LAPHi MCs promote tumor growth and offer therapeutic intervention to target these cells in cancer.

2021-11-24 | GSE174077 | GEO

Myeloid cell subsets that express latency-associated peptide promote cancer growth by modulating T cells.

Project description:Myeloid suppressor cells promote tumor growth by a variety of mechanisms which are not fully characterized. We identified myeloid cells (MCs) expressing the latency-associated peptide (LAP) of TGF-β on their surface and LAPHi MCs that stimulate Foxp3+ Tregs while inhibiting effector T cell proliferation and function. Blocking TGF-β inhibits the tolerogenic ability of LAPHi MCs. Furthermore, adoptive transfer of LAPHi MCs promotes Treg accumulation and tumor growth in vivo. Conversely, anti-LAP antibody, which reduces LAPHi MCs, slows cancer progression. Single-cell RNA-Seq analysis on tumor-derived immune cells revealed LAPHi dominated cell subsets with distinct immunosuppressive signatures, including those with high levels of MHCII and PD-L1 genes. Analogous to mice, LAP is expressed on myeloid suppressor cells in humans, and these cells are increased in glioma patients. Thus, our results identify a previously unknown function by which LAPHi MCs promote tumor growth and offer therapeutic intervention to target these cells in cancer.

| S-EPMC8602030 | biostudies-literature

Memory CD4+ T cell subsets show differential responses to HIV latency reversing agents [LARA]

Project description:HIV-1 persists in individuals on ART in infected central (CM), transitional (TM) and effector memory (EM) CD4+ T cells. We developed LARA (latency and reversion assay), which facilitates the examination of HIV latency reversal in CM, TM and EM subsets in a single assay. Studies with latency reversing agents (LRAs) revealed responses specific to each subset, including compounds that significantly reversed latency in all subsets but with a range of efficiency (bryostatin) to those that demonstrated subset specificity (IL-15). Significantly, LARA has allowed the demonstration that EM cells display a more activated profile compared to CM, which translated to enhanced efficiency in responsiveness to multiple LRAs and allowed the identification of mechanisms associated with the compounds that reactivate latent HIV in all subsets. Understanding the responsiveness of memory CD4+ T cells subsets to LRAs will accelerate the development of anti-latency therapy to interfering with viral persistence in vivo.

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Memory CD4+ T cell subsets show differential responses to HIV latency reversing agents

Project description:Memory CD4+ T cell subsets show differential responses to HIV latency reversing agents

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