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Single-cell and spatial transcriptomics reveals memory CD8+ T cell differentiation fostered by monocytes through TGF-β signaling

ABSTRACT: Single-cell and spatial transcriptomics reveals memory CD8+ T cell differentiation fostered by monocytes through TGF-β signaling

PROVIDER: PRJNA1107940 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28901340_1.fastq.gz	Fastqsanger.gz
	SRR28901340_2.fastq.gz	Fastqsanger.gz
	SRR28901341_1.fastq.gz	Fastqsanger.gz
	SRR28901341_2.fastq.gz	Fastqsanger.gz

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Single-cell and spatial transcriptomics reveals memory CD8+ T cell differentiation fostered by monocytes through TGF-β signaling

Project description:Upon antigen recognition, CD8+ T cells undergo a robust expansion and differentiation to give rise to effector and memory CD8+ T cells. The spatial determinants for effector and memory CD8+ T cell fate decision during acute infection is poorly understood. By integrating single-cell RNA sequencing (scRNA-seq) and spatial resolved transcriptomics, we investigated the anatomical locations, cell-cell interactions and molecular mechanisms that contribute to memory CD8+ T cell differentiation. We found naïve CD8+ T cells adopted a divergent differentiation trajectory where they rapidly differentiated into memory precursors (MP) and IFN-responsive cells which represent the entry point of effector T cell lineage.In the spleen, monocytes were largely colocalized with CD8+ MP cells in an antigen stimulation-dependent manner. CD8+ T cells primed with monocytes, compared to DC populations, had significantly increased memory T cell differentiation. Mechanistically, monocytes promoted memory CD8+ T cell differentiation by providing TGF-β signaling. Our study reveals a novel spatial mechanism for memory CD8+ T cell fate decision, shedding lights on the importance of monocytes and TGF-β in fostering memory CD8+ T cell development.

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Dynamics of hippocampal protein expression during long-term spatial memory formation

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Fractionated Proton Irradiation does not Impair Hippocampal Dependent Short Term or Spatial Memory in Female Mice

Project description:The environment outside the Earth’s protective magnetosphere is a much more threatening and complex space environment. The dominant causes for radiation exposure, solar particle events and galactic cosmic rays, contain high-energy protons. In space, astronauts need healthy and highly functioning cognitive abilities, of which the hippocampus plays a key role. Therefore, understanding the effects of 1H exposure on hippocampal-dependent cognition is vital for de-veloping mitigative strategies and protective countermeasures for future missions. To investi-gate these effects, we subjected 6-month-old female CD1 mice to 0.75 Gy fractionated 1H (250 MeV) whole-body irradiation at the NASA Space Radiation Laboratory. The cognitive perfor-mance of the mice was tested 3 months after irradiation using Y-maze and morris water maze tests. Both sham-irradiated and 1H-irradiated mice significantly preferred exploration of the novel arm compared to the familiar and start arms, indicating intact spatial and short-term memory. Both groups statistically spent more time in the target quadrant, indicating spatial memory retention. There were no significant differences in neurogenic and gliogenic cell counts after irradiation. In addition, proteomic analysis revealed no significant upregulation or down-regulation of proteins related to behavior, neurological disease, or neural morphology. Our data suggests 1H exposure does not impair hippocampal-dependent spatial or short-term memory in female mice.

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T-bet Suppresses TGF-b-independent Gut-resident Memory CD8+ T Cell Differentiation.

Project description:T-bet Suppresses TGF-b-independent Gut-resident Memory CD8+ T Cell Differentiation.

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Cancer-associated Fibroblast Spatial Heterogeneity and EMILIN1 Expression in Cancer Stroma Modulate TGF-b Activity and CD8+ T-Cell Infiltration in Breast Cancer

Project description:The tumor microenvironment (TME) and its multifaceted interactions with cancer cells are major targets for cancer treatment. Single-cell technologies have brought major insights into the TME, but the resulting complexity frequently precludes conclusions on function. Therefore, we combined single-cell RNA sequencing and spatial transcriptomic data to explore the relationship between different cancer-associated fibroblast (CAF) populations and immune cell exclusion in breast tumors. Our data show for the first time the degree of spatial organization of different CAF populations in breast cancer. We found that IL-iCAFs, Detox-iCAFs, and IFNγ-iCAFs tended to cluster together, while Wound-myCAFs, TGFb-myCAFs, and ECM-myCAFs formed another group that overlapped with elevated TGF-b signaling. Differential gene expression analysis of areas with CD8+ T-cell infiltration/exclusion within the TGF-b signaling-rich zones identified elastin microfibrillar interface protein 1 (EMILIN1) as a top modulated gene. EMILIN1, a TGF-b inhibitor, was upregulated in IFNγ-iCAFs directly modulating TGFb immunosuppressive function. Histological analysis of 74 breast cancer samples confirmed that high EMILIN-1 expression in the tumor margins was related to high CD8+ T-cell infiltration, consistent with our spatial gene expression analysis. High EMILIN-1 expression was also associated with better prognosis of patients with breast cancer, underscoring its functional significance for the recruitment of cytotoxic T cells into the tumor area. In conclusion, our data show that correlating TGF-b signaling to a CAF subpopulation is not enough because proteins with TGF-b-modulating activity originating from other CAF subpopulations can alter its activity. Therefore, therapeutic targeting should remain focused on biological processes rather than on specific CAF subtypes.

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