Antigen presenting cells of myeloid origin
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE2215 | GEO | 2017/12/21
SECONDARY ACCESSION(S): PRJNA91331
REPOSITORIES: GEO
Similar Datasets
Project description:Assessing the gene expression repertoire of antigen presenting dendritic cells Keywords: other
2004-09-30 | GSE702 | GEO
Project description:We isolated PBMC from healthy, moderate ( Oxygen supply < 10L/min), and severe (Oxygen supply >= 10L/min) COVID-19 patients after their admission to Intensive Care Units (ICU), at two timepoints (Day-1 and Day-4); and performed both CD14+ Monocyte enrichment followed by a Pan-DC kit to retrieve all Antigen Presenting Cell (APC) subsets from these age-matched patients. We performed single cell RNA sequencing using 10X technology on the single cell suspensions and constracted a high-resolution map of 81,643 Antigen Presenting Cells (APC) from the three COVID-19 severity groups. We were able to retrieve all the known six APC subsets and deciphered the altered pathways and ati-viral mechanisms, correlated with the disease severity.
2021-05-10 | GSE169346 | GEO
Project description:Antigen presenting cells (APC) play a central role in the host immune response to pathogen invasion by triggering early innate responses and facilitating the subsequent adaptive immune system for effective control and clearance of the infection. Accordingly, APC critically impact the outcome of an immune response. In vitro bone marrow (BM) derived APC facilitate studies aimed at dissecting their biology and function. BM derived cell cultures differentiated with granulocyte-macrophage colony stimulating factor (GM-CSF) consists of a heterogeneous mix of both dendritic cells (DC) and macrophages (MØ). Here we addressed the question of the impact of heterogeneous APC populations in their response to RNA viruses using the well characterised lymphocytic choriomeningitis virus (LCMV) infection model of BMDC populations. We compared LCMV infection and treatment with the dsRNA mimic poly (I:C)) to characterise the response of different subsets of BMDC using single cell transcriptomic analysis. Our results identified differences in the transcriptional response of BM derived APC to LCMV and poly (I:C). BM-DC were more effective at antigen presentation to T cells, whereas BM-MØ were efficient cytokine producers.
2023-12-31 | GSE193255 | GEO
Project description:Antigen presenting cells (APC) are a heterogenous population, comprised of macrophages/monocytes (CD14+ cells), classical dendritic cells (CD141+DC and CD1c+ DC) and pDC. Upon stimulation, APC migrate from peripheral organs to lymph nodes, where they drive T cell specific lineage fate, that is towards immune activation or suppression. APC in human tissues remain poorly defined. Through our previous published data we have charactised APC within adult skin and blood. Here we extend these findings, by increasing the sample for skin CD14+ DC and CD1c+ DC and performing gene array analysis of adult spleen CD14+ DC, CD141+DC and CD1c+ DC. Once, we were confident we could clearly distinguish our populations (CD14+ cell, CD141+ DC and CD1c+ DC) of interest from other cells, we sorted FACS purified the cells and prepared them for gene array analysis. Through generating subset specific gene signatures and comparing CMAP scores we confirmed we had identified equivalent APC subsets across human adult skin and spleen.
2016-12-19 | GSE85305 | GEO
Project description:BACKGROUND: Combination antiretroviral therapy (cART) is able to control HIV-1 viral replication, however long-lived latent infection in resting memory CD4+ T-cells persist. The mechanisms for establishment and maintenance of latent infection in resting memory CD4+ T-cells remain unclear. Previously we have shown that HIV-1 infection of resting CD4+ T-cells co-cultured with CD11c+ myeloid dendritic cells (mDC) produced a population of non-proliferating T-cells with latent infection. Here we asked whether different antigen presenting cells (APC), including subpopulations of DC and monocytes, were able to induce post-integration latent infection in resting CD4+ T-cells, and examined potential cell interactions that may be involved using RNA-seq. RESULTS: mDC (CD1c+), SLAN+ DC and CD14+ monocytes were most efficient in stimulating proliferation of CD4+ T-cells during syngeneic culture and in generating post-integration latent infection in non-proliferating CD4+ T-cells following HIV-1 infection of APC-T-cell co-cultures. In comparison, plasmacytoid DC (pDC) and B-cells did not induce latent infection in APC-T-cell co-cultures. We compared the RNA expression profiles of APC subpopulations that could and could not induce latency in non-proliferating CD4+ T-cells. Gene expression analysis, comparing the mDC, SLAN+ DC and CD14+ monocyte subpopulations to pDC identified 53 upregulated genes that encode proteins expressed on the plasma membrane that could signal to CD4+ T-cells via cell-cell interactions (32 genes), immune checkpoints (IC) (5 genes), T-cell activation (9 genes), regulation of apoptosis (5 genes), antigen presentation (1 gene) and through unknown ligands (1 gene). CONCLUSIONS: APC subpopulations from the myeloid lineage, specifically mDC subpopulations and CD14+ monocytes, were able to efficiently induce post-integration HIV-1 latency in non-proliferating CD4+ T-cells in vitro. Inhibition of key pathways involved in mDC-T-cell interactions and HIV-1 latency may provide novel targets to eliminate HIV latency. mRNA profiles of sorted, pure antigen presenting cells including, CD1c+ myleoid dendirtic cells (mDC), SLAN+ mDC, CD14+ monocytes and plasmacytoid DC (pDC), were generated using next generation sequencing in triplicate, using Illumina Illumina Hiseq 2000.
2015-12-23 | E-GEOD-70106 | biostudies-arrayexpress
Project description:Analysis of lung CD11c+ antigen presenting cells (APCs) isolated from wildtype or Mir22-/- mice exposed to nanoparticulate carbon black (nCB) for one month. MiR-22 plays important roles in nCB induced experimental emphysema through regulating APC activation. Results provide insight into the biological role and target genes of miR-22. Smoking-related emphysema is a chronic inflammatory disease driven by T helper 17 (TH17) cells through molecular mechanisms that remain obscure. Here we have explored the role of microRNA-22 (miR-22) in emphysema. MiR-22 was upregulated in lung myeloid dendritic cells (mDCs) of smokers with emphysema and antigen-presenting cells (APCs) of mice exposed to smoke or nanoparticulate carbon black (nCB) through a mechanism involving NF-kappaB. MiR-22-deficient mice, but not wild-type, showed attenuated TH17 responses and failed to develop emphysema after exposure to either smoke or nCB. We further show that miR-22 controls APC activation and TH17 responses through activation of AP-1 transcription factor complexes and histone deacetylase (HDAC) 4. Thus, miR-22 is a critical regulator of both emphysema and TH17 responses. Lung APCs were isolated from PBS (reference groups) or nCB exposed wildtype or Mir22-/- mice, total four groups. There were three replicates in each group.
2015-09-05 | E-GEOD-72734 | biostudies-arrayexpress
Project description:Oral tolerance prevents pathological inflammatory responses towards innocuous foreign antigens via peripheral regulatory T cells (pTreg cells). However, whether a particular subset of antigen-presenting cells (APCs) is required during dietary antigen exposure to instruct naïve CD4+ T cells to differentiate into pTreg cells has not been defined. Using myeloid lineage-specific APC depletion in mice, we found that monocyte-derived APCs are dispensable, while classical dendritic cells (cDCs) are critical for pTreg cell induction and oral tolerance. CD11b¬â cDCs from the gut-draining lymph nodes efficiently induced pTreg cells, and conversely, loss of IRF8-dependent CD11bâ cDCs impaired their polarization, although oral tolerance remained intact. These data reveal the hierarchy of cDC subsets in pTreg cell induction and their redundancy during oral tolerance development. Four dendritic cell subpopulations from mouse mesenteric lymphnodes were sorted and compared in their gene expression profile
2016-03-28 | E-GEOD-77303 | biostudies-arrayexpress
Project description:Antigen presenting cells (APC) are a heterogenous population, comprised of macrophages/monocytes (CD14+ cells), classical dendritic cells (CD141+DC and CD1c+ DC) and pDC. Upon stimulation, APC migrate from peripheral organs to lymph nodes, where they drive T cell specific lineage fate, that is towards immune activation or suppression. APC in human tissues remain poorly defined. Through our previous published data we have charactised APC within adult skin and blood. Here we extend these findings, by performing microarray analysis of adult lung CD14+ DC, CD141+ DC and CD1c+ DC. Once, we were confident we could clearly distinguish the populations of interest (CD14+ cell, CD141+ DC and CD1c+ DC) from other cells, we sorted FACS purified the cells and prepared them for gene array analysis.
2016-12-19 | GSE87494 | GEO
Project description:Oral tolerance prevents pathological inflammatory responses towards innocuous foreign antigens via peripheral regulatory T cells (pTreg cells). However, whether a particular subset of antigen-presenting cells (APCs) is required during dietary antigen exposure to instruct naïve CD4+ T cells to differentiate into pTreg cells has not been defined. Using myeloid lineage-specific APC depletion in mice, we found that monocyte-derived APCs are dispensable, while classical dendritic cells (cDCs) are critical for pTreg cell induction and oral tolerance. CD11b¬â?? cDCs from the gut-draining lymph nodes efficiently induced pTreg cells, and conversely, loss of IRF8-dependent CD11bâ?? cDCs impaired their polarization, although oral tolerance remained intact. These data reveal the hierarchy of cDC subsets in pTreg cell induction and their redundancy during oral tolerance development. Sorted naïve CD45.1 OT-II CD4 T cells were co-cultured with four dendritic cell subpopulations sorted from mouse mesenteric lymphnodes. 24h later OT-II cells were sorted again and compared in their gene expression profile.
2016-03-28 | E-GEOD-77304 | biostudies-arrayexpress
Project description:Analysis of lung CD11c+ antigen presenting cells (APCs) isolated from wildtype or Mir22-/- mice exposed to nanoparticulate carbon black (nCB) for one month. MiR-22 plays important roles in nCB induced experimental emphysema through regulating APC activation. Results provide insight into the biological role and target genes of miR-22. Smoking-related emphysema is a chronic inflammatory disease driven by T helper 17 (TH17) cells through molecular mechanisms that remain obscure. Here we have explored the role of microRNA-22 (miR-22) in emphysema. MiR-22 was upregulated in lung myeloid dendritic cells (mDCs) of smokers with emphysema and antigen-presenting cells (APCs) of mice exposed to smoke or nanoparticulate carbon black (nCB) through a mechanism involving NF-kappaB. MiR-22-deficient mice, but not wild-type, showed attenuated TH17 responses and failed to develop emphysema after exposure to either smoke or nCB. We further show that miR-22 controls APC activation and TH17 responses through activation of AP-1 transcription factor complexes and histone deacetylase (HDAC) 4. Thus, miR-22 is a critical regulator of both emphysema and TH17 responses.
2015-09-05 | GSE72734 | GEO