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Tim-4+ Cavity-Resident Macrophages Impair Anti-Tumor CD8+ T cell Immunity [RNA-Seq]

ABSTRACT: Tim-4+ Cavity-Resident Macrophages Impair Anti-Tumor CD8+ T cell Immunity [RNA-Seq]

PROVIDER: PRJNA728599 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14479948_1.fastq.gz	Fastqsanger.gz
	SRR14479948_2.fastq.gz	Fastqsanger.gz
	SRR14479949_1.fastq.gz	Fastqsanger.gz
	SRR14479949_2.fastq.gz	Fastqsanger.gz
	SRR14479950_1.fastq.gz	Fastqsanger.gz

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Tim-4+ Cavity-Resident Macrophages Impair Anti-Tumor CD8+ T cell Immunity

Project description:Tim-4+ Cavity-Resident Macrophages Impair Anti-Tumor CD8+ T cell Immunity

| PRJNA728903 | ENA

Tim-4+ Cavity-Resident Macrophages Impair Anti-Tumor CD8+ T cell Immunity [scRNA-Seq]

Project description:Tim-4+ Cavity-Resident Macrophages Impair Anti-Tumor CD8+ T cell Immunity [scRNA-Seq]

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Tim-4+ Cavity-Resident Macrophages Impair Anti-Tumor CD8+ T cell Immunity [RNA-Seq]

Project description:Here we report RNA sequencing data from sorted Tim-4low vs Tim-4high macrophages in steady-state (no tumor) mice and also MC38-LG-tumor-bearing animals that were treated with isotype or anti-Tim-4 antibody.

2021-05-12 | GSE174151 | GEO

Tim-4+ Cavity-Resident Macrophages Impair Anti-Tumor CD8+ T cell Immunity

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-05-12 | GSE174243 | GEO

Tim-4<sup>+</sup> cavity-resident macrophages impair anti-tumor CD8<sup>+</sup> T cell immunity.

Project description:Immune checkpoint blockade (ICB) has been a remarkable clinical advance for cancer; however, the majority of patients do not respond to ICB therapy. We show that metastatic disease in the pleural and peritoneal cavities is associated with poor clinical outcomes after ICB therapy. Cavity-resident macrophages express high levels of Tim-4, a receptor for phosphatidylserine (PS), and this is associated with reduced numbers of CD8+ T cells with tumor-reactive features in pleural effusions and peritoneal ascites from patients with cancer. We mechanistically demonstrate that viable and cytotoxic anti-tumor CD8+ T cells upregulate PS and this renders them susceptible to sequestration away from tumor targets and proliferation suppression by Tim-4+ macrophages. Tim-4 blockade abrogates this sequestration and proliferation suppression and enhances anti-tumor efficacy in models of anti-PD-1 therapy and adoptive T cell therapy in mice. Thus, Tim-4+ cavity-resident macrophages limit the efficacy of immunotherapies in these microenvironments.

| S-EPMC9115604 | biostudies-literature

Tim-4+ Cavity-Resident Macrophages Impair Anti-Tumor CD8+ T cell Immunity [scRNA-Seq]

Project description:Here we report transcriptional and TCR specificities associated with PSlow and PShigh CD8 T cells.

2021-05-12 | GSE174241 | GEO

Expression analysis of Tim-3 knockdown RAW264.7 cell

Project description:Investigation of whole genome gene expression level changes in a Tim-3 knockdown RAW264.7 cell, compared to control siRNA transfected RAW264.7 cell. The Tim-3 knockdown of this cell render it hyper-reactive to TLR stimulation. Tim-3 knockdown analyzed in this study are further described in Li Y, Feng J, Geng S, Geng S, Wei H, Chen G, Li X, Wang L, Wang R, Peng H, Han G, Shen B, Li Y. 2011. The N- and C-terminal carbohydrate recognition domains of galectin-9 contribute differently to its multiple functions in innate immunity and adaptive immunity. Mol Immunol. 48(4):670-7. (PID 21146220) A six chip study using total RNA recovered from Tim-3 knockdown and control RAW264.7 cells. There are 135,000 probes in a chip,each chip measures the expression level of 27526 genes of mouse from Nimblegen. Fold-change screening between the two groups obtained from the experiment. The threshold used to screen up or down regulated genes is Fold changeM-oM-<M-^-oM-<M-^]2.0

2012-12-05 | E-GEOD-42729 | biostudies-arrayexpress

Tissue-resident macrophages in the intestine are long-lived and defined by Tim-4 and CD4 expression

Project description:A defining feature of resident gut macrophages is their high replenishment rate from blood monocytes, attributed to tonic commensal-stimulation of this site. In contrast, almost all other tissues contain locally maintained macrophage populations, which co-exist with monocyte-replenished cells at homeostasis. Here, we identified three transcriptionally distinct murine gut macrophage subsets that segregate based on expression of Tim-4 and CD4. Challenging current understanding, Tim-4+CD4+ gut macrophages were found to be locally maintained, while Tim-4–CD4+ macrophages had a slow turnover from blood monocytes; indeed, Tim-4–CD4– macrophages were the only subset with the high monocyte-replenishment rate currently attributed to gut macrophages. Moreover, all macrophage subpopulations required a live microbiota to sustain their numbers, not only those derived from blood monocytes. These findings oppose the prevailing paradigm that all macrophages in the adult murine gut rapidly turnover from monocytes in a microbiome-dependant manner; instead, supplanting it with a model of ontogenetic diversity, where locally maintained subsets co-exist with rapidly replaced, monocyte-derived populations.

2018-05-15 | GSE114434 | GEO

TIM-3 restrains anti-tumour immunity by regulating inflammasome activation.

Project description:TIM-3 restrains anti-tumour immunity by regulating inflammasome activation.

| PRJNA637635 | ENA

Expression analysis of Tim-3 knockdown RAW264.7 cell

2012-12-05 | GSE42729 | GEO