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XCR1+ Dendritic Cell-Induced CD4+ T Helper-1 Activation Leads to Exacerbation of Remodeling after Myocardial Infarction

ABSTRACT: Th1 is the predominant phenotype during the early stage of MI. XCR1+ cDC1 activated CXCR3+ Th1 could be a novel therapeutic target for ischemic cardiac remodeling.

ORGANISM(S): Mus musculus

PROVIDER: GSE195915 | GEO | 2023/02/06

REPOSITORIES: GEO

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XCR1+ Dendritic Cell-Induced CD4+ T Helper-1 Activation Leads to Exacerbation of Remodeling after Myocardial Infarction (T cell research)

Project description:Th1 is the predominant phenotype during the early stage of MI. XCR1+ cDC1 activated CXCR3+ Th1 could be a novel therapeutic target for ischemic cardiac remodeling.

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XCR1 expression distinguishes human conventional dendritic cells type 1 with full effector functions from their immediate precursors

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XCR1+ Dendritic Cell-Induced CD4+ T Helper-1 Activation Leads to Exacerbation of Remodeling after Myocardial Infarction

Project description:XCR1+ Dendritic Cell-Induced CD4+ T Helper-1 Activation Leads to Exacerbation of Remodeling after Myocardial Infarction

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Regulation of gene expression in splenic cDC1 isolated from WT vs XCR1-/- miceNK cells orchestrate cDC1 migration to potentiate antiviral protective CD8+ T cell responses

Project description:The expression of the XCR1 chemokine receptor univocally identifies all type 1 conventional dendritic cells (cDC1) throughout the body. The gene encoding its ligand, XCL1, is expressed constitutively by innate lymphoid cells such as natural killer (NK) cells. The evolutionary conservation of XCR1, XCL1 in vertebrates suggests that they play a critical, yet uncharacterized, role in immune responses. Here we showed using mouse cytomegalovirus (MCMV) infection, that the XCL1/XCR1 axis promoted the intra-splenic repositioning of cDC1 towards IFN--producing NK cells forming superclusters around infected cells. There, cDC1 and NK cells engaged into physical interactions enhancing their respective production of IL-12 and IFN-. This feed-forward mechanism also led to NK cell production of GM-CSF, which upregulated CCR7 on cDC1, instructing them to migrate into the T cell area for the priming of CD8+ T cells. In conclusion, we identified a novel mechanism through which NK cells boost the relay between innate and adaptive immunities by regulating the spatiotemporal functions of cDC1.

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FACS–array profiling of helper T cell subtypes from human peripheral blood.

Project description:Gene expression analysis of Th1(CD4+/CXCR3+/CCR4-) and Th2 ((CD4+/CCR4+/CXCR3-) cells by FACS-array 12 Th1 and 12 Th2 samples

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XCR1+ Dendritic Cell-Induced CD4+ T Helper-1 Activation Leads to Exacerbation of Remodeling after Myocardial Infarction (T cell research)

Project description:XCR1+ Dendritic Cell-Induced CD4+ T Helper-1 Activation Leads to Exacerbation of Remodeling after Myocardial Infarction (T cell research)

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FACS–array profiling of helper T cell subtypes from human peripheral blood.

Project description:Gene expression analysis of Th1(CD4+/CXCR3+/CCR4-) and Th2 ((CD4+/CCR4+/CXCR3-) cells by FACS-array

2014-11-13 | GSE59295 | GEO

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Thymic XCR1+ dendritic cells undergo a functional maturation fundamentally similar to that of peripheral tolerogenic XCR1+ dendritic cells

Project description:Dendritic cells (DC) play critical roles in central and peripheral T cell tolerance. DC found in the steady-state periphery undergo an homeostatic, tolerogenic, maturation that promotes interaction with naive T cells and induction of abortive responses. In contrast, thymic DC are thought to exist solely in an immature state. In this study, we show that XCR1+ thymic DC constitutively mature into a stage characterized by high levels of molecules involved in T cell activation. This unanticipated mature stage corresponded to a third of the XCR1+ thymic DC and fully accounted for their ability to cross-present self-antigens to developing T cells. Transcriptomic analysis of the XCR1+ DC found in thymus and steady-state periphery revealed that their maturation involves profound and convergent changes. Unexpectedly, maturation resulted in down-regulation of genes conferring their specific function on XCR1+ DC. Paradoxically, upon maturation, central and peripheral tolerogenic XCR1+ DC up-regulated many genes thought to drive pro-inflammatory T-cell responses. Thus, our results reveal that thymic XCR1+ DC undergo constitutive maturation and emphasize the common mechanisms operating for both central and peripheral tolerance induction by XCR1+ DC. DC were isolated from lymphoid organs as previously described (Vremec et al., 2000). DC subsets were sorted by flow cytometry according to the marker combinations described in the âcharacteristics: phenotypeâ field for each sample.

2016-08-22 | E-GEOD-71166 | biostudies-arrayexpress

miRNA expression data from human myocardial infarction hearts

Project description:Sexual dimorphisms are well recognized in various cardiac diseases, including myocardial infarction (MI). MI develops later in women, but once established, it contributes more persistent symptoms and higher mortality than in men. Although mRNA-level sexual dimorphism of MI have been reported, whether miRNA transcriptome also confers such dimorphism remains unknown. Comprehensive understanding of the mRNA- and miRNA-level genetic programs underlying the heart sexual dimorphisms will expectedly improve clinical outcome by facilitating the development of gender specific treatment strategies. Here, by conducting miRNA microarray analysis of human MI samples, we set out to characterize the heart sexual dimorphisms at the level of miRNA transcriptome Human tissue samples, acquired during post-mortem examination and frozen in liquid nitrogen, were provided by the department of pathology, Tokyo Metropolitan Geriatric Hospital after the approval from the ethical committee. Age- and sex-matched cohorts were selected to compare healthy hearts to those with post-MI LV remodeling. Border zone for myocardial infarction was sampled. Total RNA was extracted using Sepasol solution (Sepasol-RNA I super G, nakalai tesque, Japan), and microarray analysis was performed using Affymetrix GeneChipÂ® miRNA 3.0 Arrays

2016-01-07 | E-GEOD-76591 | biostudies-arrayexpress

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