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Acquisition of residency programs by T cells entering the human brain

ABSTRACT: Acquisition of residency programs by T cells entering the human brain

PROVIDER: PRJNA1207021 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31902000_1.fastq.gz	Fastqsanger.gz
	SRR31902000_2.fastq.gz	Fastqsanger.gz
	SRR31902001_1.fastq.gz	Fastqsanger.gz
	SRR31902001_2.fastq.gz	Fastqsanger.gz
	SRR31902002_1.fastq.gz	Fastqsanger.gz

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Acquisition of residency programs by T cells entering the human brain

Project description:Surveillance by T cells is mandatory for maintaining a healthy state of the central nervous system (CNS), while aberrant accumulation of T cells is linked to neuroinflammatory diseases. To understand the phenotype of T cells recruited into distinct CNS compartments, we studied CD8+ and CD4+ T cells isolated from CNS border compartments (choroid plexus and meninges), intrathecal compartments (cerebrospinal fluid (CSF) and subcortical white matter (WM)), and paired peripheral blood of human brain donors. Flow-cytometric analyses revealed that T cells in all CNS compartments show an effector memory phenotype. Tissue residency-associated integrins (CD49a, CD103), chemokine receptors (CCR2, CCR5), and brain T cell-associated CD20, but not the canonical tissue resident memory T-cell marker CD69, were enriched in T cells from both CNS border compartments compared to blood. While small circulating fractions co-expressed these border-associated markers, the interaction of T cells with brain endothelium resulted in up-regulation of CD49a and CD103, with a further gain of CD20 upon trans-endothelial migration. In contrast to border compartments, intrathecal T cells were additionally characterized by a high expression of CD69. The transcriptomes of intrathecal T cells from CSF and WM were very similar and displayed a tissue residency-associated pattern. Still, WM-derived T cells showed a lower expression of markers associated with migratory potential (CRTAM, RGS1), recent activation (CD25, HLA-DR), and co-stimulation (CD28), which was associated with reduced Eomes expression. This work demonstrates the versatility of T-cell phenotypes across CNS compartments and provides insight into the programs regulating their recruitment and maintenance within the CNS.

2025-05-26 | GSE285938 | GEO

Metabolic Programs of T Cell Tissue Residency Empower Tumor Immunity

Project description:Metabolic Programs of T Cell Tissue Residency Empower Tumor Immunity

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Metabolic Programs of T Cell Tissue Residency Empower Tumor Immunity [Human scRNA-seq]

Project description:Metabolic Programs of T Cell Tissue Residency Empower Tumor Immunity [Human scRNA-seq]

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Metabolic Programs of T Cell Tissue Residency Empower Tumor Immunity [Human scRNA-seq]

Project description:Tissue-resident memory CD8 T cells (TRM) offer fast, robust, and long-term protection at sites of re-infection1. Tumor-infiltrating lymphocytes (TIL) with characteristics of TRM maintain enhanced effector functions, predict responses to immunotherapy, and accompany better prognoses2,3. Thus, an improved understanding of the metabolic strategies that enable tissue residency could inform new approaches to empower T cell responses in tissues and solid tumors. To systematically define the basis for the metabolic reprogramming supporting TRM differentiation, survival, and function, we leveraged in vivo functional genomics, untargeted metabolomics, and transcriptomics of virus-specific memory CD8 T cell populations. We found that memory CD8 T cells deployed a range of adaptations to tissue residency, including a marked reliance on non-steroidal products of the mevalonate/cholesterol pathway, such as Coenzyme Q (CoQ), driven by increased activity of the transcription factor Srebp2. This metabolic adaptation was most pronounced in the small intestine (SI), where TRM interface with dietary cholesterol and maintain a heightened state of activation4, and was shared by functional TIL in diverse tumor types in mice and humans. Enforcing CoQ synthesis through Fdft1 deletion or Pdss2 overexpression promoted mitochondrial respiration, memory formation upon viral infection, and enhanced antitumor immunity. In sum, through a systematic exploration of TRM metabolism, we reveal how these programs can be leveraged to empower CD8 T cell memory formation in the context of acute infections and enhance antitumor immunity.

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Metabolic Programs of T Cell Tissue Residency Empower Tumor Immunity [scRNA-seq]

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Runx3 programs CD8+ T cell residency in non-lymphoid tissues and tumours

Project description:Runx3 programs CD8+ T cell residency in non-lymphoid tissues and tumours

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Metabolic Programs of T Cell Tissue Residency Empower Tumor Immunity [RNA-seq]

Project description:Metabolic Programs of T Cell Tissue Residency Empower Tumor Immunity [RNA-seq]

| PRJNA853360 | ENA

Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency

Project description:Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency

| PRJNA1160824 | ENA

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Project description:Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency [dnRA_Antag]

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