E-MEXP-3726
Ontology highlight
ABSTRACT:
PROVIDER: E-MEXP-3726 | ExpressionAtlas | 2015-06-05
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MEXP-3726-analysis-methods.tsv | Tabular | |||
| E-MEXP-3726-atlasExperimentSummary.Rdata | Rdata | |||
| E-MEXP-3726-configuration.xml | Xml | |||
| E-MEXP-3726-percentile-ranks.tsv | Tabular | |||
| E-MEXP-3726.condensed-sdrf.tsv | Tabular |
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Project description:Natural regulatory T cells (nTregs) are known to increase during chronic infection or at the site tumor, though the exact mechanisms that contribute to their accumulation and mode of action remain unclear. We used flow cytometry and microarray analyses to delineate the phenotype of nTregs and their role in modulating T cell and antigen presenting cell (APC) function in the setting of chronic infection. Using cells from 18 filaria-infected (Fil+) and 19 filaria-uninfected (Fil-) subjects, we found that the frequencies of nTreg expressing CTLA-4, GITR, LAG-3, and IL-10 were significantly higher in Fil+ compared with Fil- subjects. Microarray analysis revealed that, compared with those from Fil-, nTreg populations in Fil+ subjects were more heterogeneous and had higher expression of IL-10, CCL-4, IL-29 and CTLA-4, molecules that have been implicated in immune suppression. Moreover, the nTregs from Fil+ subjects had markedly upregulated activation-induced apoptotic genes with concomitant down regulation of cell survival genes. However, these activated nTregs from Fil+ subjects did not significantly affect cytokine production by APCs. To determine if nTregs directly modulate APC function, we modeled an in vitro culture system with cells from normal individuals. In this system, in response to antigen or anti-CD3, nTregs did inhibit APC production of IL-12-, CXCL-9, and CXCL-10, but did so indirectly through effector T cells. Taken together, our results suggest that in filarial infection, the expanded nTreg populations are heterogeneous, short-lived, activated and express regulatory molecules that modulate cytokine production by APC indirectly through an effector T cell-dependent mechanism.
2016-02-25 | GSE44767 | GEO
Project description:Natural regulatory T cells (nTregs) are known to increase during chronic infection or at the site tumor, though the exact mechanisms that contribute to their accumulation and mode of action remain unclear. We used flow cytometry and microarray analyses to delineate the phenotype of nTregs and their role in modulating T cell and antigen presenting cell (APC) function in the setting of chronic infection. Using cells from 18 filaria-infected (Fil+) and 19 filaria-uninfected (Fil-) subjects, we found that the frequencies of nTreg expressing CTLA-4, GITR, LAG-3, and IL-10 were significantly higher in Fil+ compared with Fil- subjects. Microarray analysis revealed that, compared with those from Fil-, nTreg populations in Fil+ subjects were more heterogeneous and had higher expression of IL-10, CCL-4, IL-29 and CTLA-4, molecules that have been implicated in immune suppression. Moreover, the nTregs from Fil+ subjects had markedly upregulated activation-induced apoptotic genes with concomitant down regulation of cell survival genes. However, these activated nTregs from Fil+ subjects did not significantly affect cytokine production by APCs. To determine if nTregs directly modulate APC function, we modeled an in vitro culture system with cells from normal individuals. In this system, in response to antigen or anti-CD3, nTregs did inhibit APC production of IL-12-, CXCL-9, and CXCL-10, but did so indirectly through effector T cells. Taken together, our results suggest that in filarial infection, the expanded nTreg populations are heterogeneous, short-lived, activated and express regulatory molecules that modulate cytokine production by APC indirectly through an effector T cell-dependent mechanism. Control (nTREG-Lymphatic Filariasis negative) vs. test (nTREG-Lymphatic Filariasis positive)
2016-02-25 | E-GEOD-44767 | biostudies-arrayexpress
Project description:Unraveling the diversity of Th2 effector cells subsets may help us to understand their pathogenic role in Type-2 associated inflammatory disorders, including allergic diseases and helminth infections. To characterize the heterogeneity and function of these effector Th2 cells, we analyzed 47 subjects’ PBMCs [23 filarial-infected (Fil+) with or without coincident HDM sensitization (Fil+HDM+ n=12; Fil+HDM-, n=11) and 24 subjects without filarial infection (Fil-) (Fil-HDM+ n=12; and Fil-HDM-, n=12) using multiparameter flow cytometry and two-level FlowSOM analysis. The frequency of 3 memory CD4+ T cell clusters, including CCR4+CCR6+CRTH2- (subset 1), CCR4+CCR6-CRTH2+ (subset 2), and CCR6+CCR4+CRTH2+ (subset 3) were markedly enriched among Fil+ subjects. The functional characterization indicated subset 2 and 3 as distinct Th2 cytokine producers, which together were responsible for the majority of IL-4, IL-5, or IL-13 produced among the Fil+ subjects. These subsets were sorted and analyzed by multiomic single cell RNA profiling. Indeed, both subset 2 and subset 3 presented features of pathogenic Th2 effector cells based on their single cell molecular signature, including downregulation of cd27 and high expression levels of itga4, il-17rb, hpgds, klrb1, ptgdr2, il-9r, il-4, il5 and il-13 genes when compared with conventional Th2 cells from healthy controls. When the Fil+ subjects were divided based on allergic status, the Fil+HDM+ subjects had an expansion of both subset 2 (3.19% vs 1.28%, p=0.001) and subset 3 (0.39% vs 0.15%, p=0.002) Th2 cells when compared with Fil+HDM-. Gene expression analysis further demonstrated that concomitant HDM sensitization in the presence of filarial infection reshaped the molecular program of these pathogenic effector Th2 subsets by even further upregulating the expression of gata3, il17rb, clrf2, and klrb1. Notably, Fil+HDM+ patients’ cells showed higher responsiveness to filarial or HDM antigenic stimulation, producing even higher levels of IL-4, IL-5 and IL-13 when compared with Fil+HDM- patients. This distinct molecular and functional program of Th2 effector cells subsets sheds new light on the Th2 cell plasticity and their contribution to immune regulation in helminth infection and allergic diseases.
2024-05-29 | GSE240865 | GEO
Project description:Facial infiltrating lipomatosis (FIL) is a congenital disorder characterized by unilateral facial enlargement. Although next-generation sequencing has revealed that the pathogenesis of FIL is associated with phosphatidylinositol 3-kinase catalytic subunit alpha (PIK3CA) mutations, the underlying molecular mechanisms remain undetermined. We found that the adipose tissue in FIL patients demonstrated tissue infiltration accompanied by adipocytes hypertrophy and increased lipid accumulation. All FIL-ADSCs harboured PIK3CA mutations. Compared to ADSCs obtained from normal subcutaneous adipose tissue, FIL-ADSCs exhibited a greater capacity for adipogenesis. Suppression of PIK3CA resulted in a reduction in the adipogenic potential of FIL-ADSCs. Furthermore, WX390, a novel dual-target PI3K/mTOR inhibitor, was found to impede PIK3CA-mediated adipogenesis both in vivo and in vitro. RNA-seq revealed that the expression of transient receptor potential vanilloid subtype 1 (TRPV1) was upregulated after PI3K pathway inhibition, and overexpression and activation of TRPV1 both inhibited adipogenesis of FIL-ADSCs. Our study showed that PIK3CA mutations promoted adipogenesis in FIL-ADSCs and that this effect was achieved by suppressing the expression of TPRV1. Pathogenesis experiments suggested that WX390 may serve as an agent for the treatment of FIL.
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Project description:BP and ER encode proteins that act synergistically to regulate Arabidopsis inflorescence architecture. To search for genes/proteins that influence the BP/ER signaling pathways, we conducted mutagenesis of the bp er double mutant and found that a mutation in FILAMENTOUS FLOWER (FIL) suppresses many of the morphological/developmental defects in bp er. Given that FIL encodes a Zn-finger containing transcription factor, microarray analysis was conducted on bp er vs. the bp er fil line to identify genes that are misregulated and which might implicate specific genes/proteins/pathways that are involved in regulating inflorescence development.
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Project description:The endoplasmic reticulum (ER) is an organelle associated with lipid metabolism. However, the involvement of the ER in nutritional status-dependent energy homeostasis is largely unknown. The results of this study demonstrate that IRE-1, an ER protein known to be involved in the unfolded protein response, and HSP-4, an ER chaperone, regulate expression of the novel fasting-induced lipases FIL-1 and FIL-2, which induce fat granule hydrolysis upon fasting in C. elegans. RNAi and ectopic expression experiments demostrated that FIL-1 and FIL-2 are both necessary and sufficient for fasting-induced fat granule breakdown. Failure of ire-1 and hsp-4 mutant animals to hydrolyze fat granules during starvation impaired their motility, which was rescued by glucose supplementation of their media, implicating the importance of ire-1/hsp-4-dependent lipolysis for energy supply from stored fat during fasting. Taken together, these data suggest that the ER-resident proteins IRE-1 and HSP-4 are key nutritional sensors that modulate expression of inducible lipases to maintain whole-body energy homeostasis in C. elegans.
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Project description:The endoplasmic reticulum (ER) is an organelle associated with lipid metabolism. However, the involvement of the ER in nutritional status-dependent energy homeostasis is largely unknown. The results of this study demonstrate that IRE-1, an ER protein known to be involved in the unfolded protein response, and HSP-4, an ER chaperone, regulate expression of the novel fasting-induced lipases FIL-1 and FIL-2, which induce fat granule hydrolysis upon fasting in C. elegans. RNAi and ectopic expression experiments demostrated that FIL-1 and FIL-2 are both necessary and sufficient for fasting-induced fat granule breakdown. Failure of ire-1 and hsp-4 mutant animals to hydrolyze fat granules during starvation impaired their motility, which was rescued by glucose supplementation of their media, implicating the importance of ire-1/hsp-4-dependent lipolysis for energy supply from stored fat during fasting. Taken together, these data suggest that the ER-resident proteins IRE-1 and HSP-4 are key nutritional sensors that modulate expression of inducible lipases to maintain whole-body energy homeostasis in C. elegans. Synchronized L4 worms were divided into well-fed and 6 hours fasted samples for RNA extraction and hybridization on an Agilent microarray.
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Project description:Facial infiltrating lipomatosis is characterized by excessive growth of adipose tissue, The etiology is associated with somatic PIK3CA variant, but the specific mechanisms are not yet fully understood. In this study, we collected facial adipose tissue from both FIL patients and non-FIL individuals, isolated the stromal vascular fraction (SVF) and performed single-cell transcriptome sequencing on these samples. We mapped out the cellular landscape within the SVF and specifically focused on a deeper analysis of fibro-adipogenic precursor cells (FAPs).
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