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

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: GSE195910 | 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

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.

2023-02-06 | GSE195915 | GEO

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

Project description:Dendritic cells (DCs) are major regulators of innate and adaptive immune responses. DCs can be classified into plasmacytoid DCs and conventional DCs (cDCs) type 1 and 2. Murine and human cDC1 share the mRNA expression of XCR1. Murine studies indicated a specific role of the XCR1-XCL1 axis in the induction of immune responses. Here, we describe that human cDC1 can be distinguished into XCR1- and XCR1+ cDC1 in lymphoid as well as non-lymphoid tissues. Steady state XCR1+ cDC1 display a pre-activated phenotype compared to XCR1- cDC1. Upon stimulation, XCR1+ cDC1, but not XCR1- cDC1, secreted high levels of inflammatory cytokines as well as chemokines. This was associated with enhanced activation of NK cells mediated by XCR1+ cDC1. Moreover, XCR1+ cDC1 excelled in inhibiting replication of Influenza A virus. Further, under DC differentiation conditions, XCR1- cDC1 developed into XCR1+ cDC1. After acquisition of XCR1 expression, XCR1- cDC1 secreted comparable level of inflammatory cytokines. Thus, XCR1 is a marker of terminally differentiated cDC1 that licenses the antiviral effector functions of human cDC1, while XCR1- cDC1 seem to represent a late immediate precursor of cDC1.

2023-07-31 | GSE237715 | GEO

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.

2021-09-22 | GSE142402 | GEO

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

2014-11-13 | E-GEOD-59295 | biostudies-arrayexpress

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

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

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

2016-08-22 | GSE71166 | GEO

XCR1+ type 1 conventional dendritic cells drive liver pathology in Non-Alcoholic Steatohepatitis [scRNA-seq]

Project description:Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are prevalent liver conditions, which underlie the development of life-threatening cirrhosis, liver failure and liver cancer. Chronic necro-inflammation is a critical factor in development of NASH, yet the cellular and molecular mechanisms of immune dysregulation in this disease are poorly understood. Here, using single cell transcriptomic analysis, we comprehensively profiled the immune composition of the mouse liver during NASH. We identified a significant pathology-associated increase in hepatic conventional dendritic cells (cDC), and further defined their source as NASH-induced boost in cycling of cDC progenitors in the bone marrow. Analysis of blood and liver from patients on the NALFD/NASH spectrum showed that cDC type 1 (cDC1) were more abundant and activated in disease. Genomic analysis of cDC-T pairs in liver draining lymph nodes revealed that cDCs in NASH promote inflammatory T cell reprogramming, previously associated with NASH worsening. Finally, depletion of cDC1 in XCR1DTA mice or using anti-XCL1 blocking antibody attenuated liver pathology in NASH mouse models. Overall, our study provides a comprehensive characterization of cDC biology in NASH, and identifies XCR1+ cDC1 as an important driver of liver pathology.

2021-05-21 | GSE169445 | GEO

XCR1+ type 1 conventional dendritic cells drive liver pathology in Non-Alcoholic Steatohepatitis [10x scRNA-seq]

2021-05-21 | GSE169446 | GEO

Transcriptional profiles of CCR7lo effector memory human T cell subsets

Project description:The aim of this study was to identify differentially-expressed genes in CCR4hi/CXCR3- and CCR4lo CXCR3+ CCR6+ human Th17 cell subsets Human CD45RO+ memory T cells isolated from the peripheral blood of healthy adult donors were sorted into 4 predominant CCR7lo CD25- effector memory subsets: (1) Th1 - CCR6- CCR4lo CXCR3+; (2) Th2 - CCR6- CCR4hi CXCR3+; (3) Th17 - CCR6+ CCR4hi CXCR3-; (4) Th17.1 - CCR6+ CCR4lo CXCR3-. Sorted cells were cultured in media and activated via anti-CD3/anti-CD28 beads for 36 hours. All subsets were then harvested and used for RNA extraction and microarray experiments. Th1 vs Th2; Th1 vs Th17; Th1 vs Th17.1; Th2 vs Th17; Th2 vs Th17.1; Th17 vs Th17.1

2013-12-17 | E-GEOD-49703 | biostudies-arrayexpress

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