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Type I interferon activates MHC class I-dressed CD11b+ conventional dendritic cells to promote protective anti-tumor CD8+ T cell immunity

ABSTRACT: Type I interferon activates MHC class I-dressed CD11b+ conventional dendritic cells to promote protective anti-tumor CD8+ T cell immunity

PROVIDER: PRJNA753929 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11950080_1.fastq.gz	Fastqsanger.gz
	SRR11950080_2.fastq.gz	Fastqsanger.gz
	SRR11950081_1.fastq.gz	Fastqsanger.gz
	SRR11950081_2.fastq.gz	Fastqsanger.gz
	SRR11950082_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Type I interferon activates MHC class I-dressed CD11b+ conventional dendritic cells to promote protective anti-tumor CD8+ T cell immunity

Project description:Tumor-infiltrating antigen-presenting cells, such as dendritic cells (DC), have the capacity to shape anti-tumor T cell responses. While tremendous progress has been made in unraveling the role of Batf3-driven DC1 in the anti-tumor immune response, the contributions of other tumor-infiltrating DC subsets remain poorly understood. Furthermore, tumor-infiltrating DC exist in a range of functional states with differential impacts on anti-tumor immunity. In this study, we sought to identify and characterize the functionally relevant DC states associated with a productive anti-tumor T cell response. By comparing the DC infiltrate of spontaneously regressing tumors and progressing tumors, we identified a novel activation state of CD11b+ conventional DC in tumors, which expressed an interferon-stimulated gene signature (‘ISG+ DC’). ISG+ DC were activated by type-I-interferon-induced signaling and could generate protective CD8+ T cell responses by cross-dressing with tumor-derived peptide-MHC complexes. Stimulatory ISG+ DC induced by exogenous IFNβ addition drove robust anti-tumor T cell responses in poorly immunogenic tumors even in the absence of DC1.

2022-01-13 | GSE181938 | GEO

Type I interferon activates MHC class I-dressed CD11b+ conventional dendritic cells to promote protective anti-tumor CD8+ T cell immunity

2022-01-13 | GSE151990 | GEO

Type I interferon activates MHC class I-dressed CD11b+ conventional dendritic cells to promote protective anti-tumor CD8+ T cell immunity

Project description:Type I interferon activates MHC class I-dressed CD11b+ conventional dendritic cells to promote protective anti-tumor CD8+ T cell immunity

| PRJNA753931 | ENA

Type I interferon activates MHC class I-dressed CD11b+ conventional dendritic cells to promote protective anti-tumor CD8+ T cell immunity

Project description:Type I interferon activates MHC class I-dressed CD11b+ conventional dendritic cells to promote protective anti-tumor CD8+ T cell immunity

| PRJNA638022 | ENA

Type I interferon activates MHC class I-dressed CD11b+ conventional dendritic cells to promote protective anti-tumor CD8+ T cell immunity

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

2022-01-13 | GSE181939 | GEO

Expression data from lung CD11b+ conventional dendritic cells in the steady-state and following exposure to house dust mite allergens

Project description:Using mouse lung resident conventional CD11b+ dendritic cells (CD11b+ cDCs) in the context of house-dust mite (HDM)-driven allergic airway sensitization as a model, we aimed here to identify transcriptional events regulating the pro-Th2 activity of cDCs. We used microarray analyses to identify genes differentially expressed by lung CD11b+ conventional dendritic cells in response to house dust mite allergens in wild-type and Irf3-deficient mice

2016-09-30 | GSE80809 | GEO

Immunopeptidomics reveals determinants of Mycobacterium tuberculosis antigen presentation on MHC class I (SureQuant data)

Project description:CD8+ T cells contribute to protective immunity to Mycobacterium tuberculosis (Mtb), but the principles that govern presentation of Mtb peptides on MHC class I (MHC-I) on the surface of infected macrophages for CD8+ T cell recognition are incompletely understood. Here, we use internal standard parallel reaction monitoring (IS-PRM, also known as SureQuant) to rigorously validate identifications of Mtb-derived MHC-I peptides obtained in data-dependent MS analyses. We further use SureQuant to quantify presentation of Mtb peptides derived from the secreted effector proteins EsxA and EsxJ across multiple experimental conditions. We show that presentation of both EsxA- and EsxJ-derived peptides requires the activity of the mycobacterial ESX-1 type VII secretion system, possibly indicating that ESX-1-mediated phagosome membrane damage allows Mtb proteins to access MHC-I antigen processing pathways. We show that this requirement is independent of type I interferon signaling that occurs downstream of phagosome damage. Treatment with inhibitors of conventional proteolytic pathways involved in MHC-I antigen processing inhibits presentation of self peptides as expected, but does not inhibit presentation of Mtb peptides, implying an alternative or redundant mechanism of processing.

2023-04-24 | PXD037843 | Pride

mhc class I_SIV

Project description:MHC class I of Chinese Rhesus Monkeys and their impact on SIV replication

| PRJEB4483 | ENA

Equine MHC class II

Project description:Sequencing and annotation of equine MHC class II region

| PRJEB15527 | ENA

MHC class I and MHC class II reporter mice enable analysis of immune oligodendroglia in mouse models of multiple sclerosis

Project description:Oligodendrocytes and their progenitors upregulate MHC pathways in response to inflammation, but the frequency of this phenotypic change is unknown and the features of these immune oligodendroglia are poorly defined. We generated MHC class I and II transgenic reporter mice to define their dynamics in response to inflammatory demyelination, providing a means to monitor MHC activation in diverse cell types in living mice and define their roles in aging, injury and disease.

2022-09-23 | GSE213739 | GEO

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