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CD4+ T cell calibration of antigen-presenting cells optimizes antiviral CD8+ T cell immunity

ABSTRACT: CD4+ T cell calibration of antigen-presenting cells optimizes antiviral CD8+ T cell immunity

PROVIDER: PRJNA720605 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14182400.fastq.gz	Fastqsanger.gz
	SRR14182401.fastq.gz	Fastqsanger.gz
	SRR14182402.fastq.gz	Fastqsanger.gz
	SRR14182403.fastq.gz	Fastqsanger.gz
	SRR14182404.fastq.gz	Fastqsanger.gz

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CD4+ T cell calibration of antigen-presenting cells optimizes antiviral CD8+ T cell immunity

Project description:Antiviral CD8+ T cell immunity depends on the integration of various contextual cues, but how antigen-presenting cells (APCs) consolidate these signals for decoding by T cells remains unclear. Here, we describe gradual interferon-α/interferon-β (IFNα/β)-induced transcriptional adaptations that endow APCs with the capacity to rapidly activate the transcriptional regulators p65, IRF1 and FOS after CD4+ T cell-mediated CD40 stimulation. While these responses operate through broadly used signaling components, they induce a unique set of co-stimulatory molecules and soluble mediators that cannot be elicited by IFNα/β or CD40 alone. This response is critical for the acquisition of antiviral CD8+ T cell effector function, and its activity in APCs from individuals infected with severe acute respiratory syndrome coronavirus 2 correlates with milder disease. These observations uncover a sequential integration process whereby APCs rely on CD4+ T cells to select the innate circuits that guide antiviral CD8+ T cell responses.

2023-02-27 | GSE171690 | GEO

Therapeutic antiviral T cells noncytopathically clear persistently infected microglia after conversion into antigen-presenting cells

Project description:Several viruses can infect the mammalian nervous system and induce neurological dysfunction. Adoptive immunotherapy (AI) is an approach that involves administration of antiviral T cells and has shown promise in clinical studies for the treatment of peripheral virus infections in humans such as cytomegalovirus, Epstein-Barr virus, and adenovirus, among others. Clearance of neurotropic infections, on the other hand, is particularly challenging because the central nervous system (CNS) is relatively intolerant of immunopathological reactions. Therefore, it is essential to develop and mechanistically understand therapies that noncytopathically eradicate pathogens from the CNS. Here, we used mice persistently infected from birth with lymphocytic choriomeningitis virus (LCMV) to demonstrate that therapeutic antiviral T cells can completely purge the persistently infected brain without causing blood brain barrier breakdown or tissue damage. Mechanistically, this is accomplished through a tailored release of chemoattractants that recruit antiviral T cells, but few pathogenic innate immune cells such as neutrophils and inflammatory monocytes. Upon arrival, T cells enlisted the support of nearly all brain resident myeloid cells (microglia) by converting them into CD11c+ antigen-presenting cells (APCs) – a cell population also found in the brain of a human immunodeficiency virus infected patient. Two-photon imaging studies revealed that antiviral CD8+ and CD4+ T cells interacted directly with CD11c+ microglia and induced STAT1 signaling, but did not initiate programmed cell death. We propose that noncytopathic CNS viral clearance can be achieved by therapeutic antiviral T cells reliant on restricted chemoattractant production and interactions with apoptosis-resistant microglia. 6 Mouse Microglia-sorted Brain Samples: 3 (-) AI, 3 (+) AI.

2015-06-22 | E-GEOD-66421 | biostudies-arrayexpress

Therapeutic antiviral T cells noncytopathically clear persistently infected microglia after conversion into antigen-presenting cells

2015-06-22 | GSE66421 | GEO

Calibration array

Project description:Calibration array

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Calibration array

Project description:Calibration array used to assess probe specific binding behaviour across eight different amounts of DNA starting material. This calibration step was performed to select one best out of three probes per gene based on probe responsiveness on increasing DNA staring material. It was further used to calibrate a subsequent microarray experiment to account for probe specific binding behaviour as part of the normalization process (see also Dennenmoser et al. 2017 Copy number increases of transposable elements and protein coding genes in an invasive fish of hybrid origin).

2017-07-01 | GSE93063 | GEO

Antigen Presenting Dendritic Cells

Project description:Assessing the gene expression repertoire of antigen presenting dendritic cells Keywords: other

2004-09-30 | GSE702 | GEO

Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells

Project description:Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells

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Delineating Tumor-infiltrating Antigen Presenting Cell populations

Project description:The goal of this study is to compare tumor-infiltrating antigen presenting cell populations by global transcriptome profiling (RNA-seq) to help further delineate sub-populations of infiltrating myeloid cells in tumor. Methods: Four tumor antigen presenting cell populations were sorted from digested B78chOVA (melanoma variant) tumors in biological triplicate Results: RNA was extracted from the 4 groups (n=3 per group) and prepared for RNAseq. Sequencing yielded ~405 million reads with an average read depth of 33.7 million reads/sample. Reads were then aligned to the mouse genome (UCSC mm10) and those that mapped uniquely to known mRNAs were used to assess differential expression.

2014-11-10 | GSE61462 | GEO

Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells [Multiome]

Project description:Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells [Multiome]

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Mapping the thymic hematopoietic antigen presenting cell network

Project description:Mapping the thymic hematopoietic antigen presenting cell network

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