Oligoarray analysis of mRNA species from DCs treated with C. parvum for 24 h.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE24121 | GEO | 2010/10/20
SECONDARY ACCESSION(S): PRJNA130059
REPOSITORIES: GEO
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Project description:To investigate whether C. parvum treatment of DCs regulates other inflammatory genes, mouse BMDCs (CD11c and CD11b positive) were treated with C. parvum for 24 hr. Control groups included untreated BMDCs and DCs treated with E. cuniculi. We noticed that a significant upregulation of the expression of interferon-related genes, which may correlation the critical role of interferon in host defense against C. parvum infection. DCs were treated with C. parvum for 24 hr. Control groups included untreated BMDCs and DCs treated with E. cuniculi. Group comparison was performed using the data of 3 replicate arrays from each time point.
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2013-09-17 | E-GEOD-50898 | biostudies-arrayexpress
Project description:Innate immune cells are integral to the pathogenesis of several diseases of the central nervous system (CNS), including multiple sclerosis (MS). Dendritic cells (DCs) are potent CD11c+ antigen presenting cells which function as critical regulators of adaptive immune responses, particularly in autoimmune diseases such as MS. The regulation of DC function in both the periphery and CNS compartment has not been fully elucidated. One limitation to studying the role of CD11c+ DCs in the CNS is that microglia have been shown to upregulate CD11c during inflammation, making it challenging to distinguish hematopoietically-derived DCs from microglia. Selective expression of microRNAs (miRNAs) has been shown to distinguish populations of innate cells within the CNS during neuro-inflammation and is proposed as a mechanism for the regulation of innate cell function. Using the experimental autoimmune encephalomyelitis (EAE) murine model of MS, we characterized the expression of miRNAs in CD11c+ cells using a non-biased murine array. Several miRNAs, including miR-31, were enriched in CD11c+ cells within the CNS during EAE, but not LysM+ microglia. Moreover, to distinguish CD11c+ DCs from microglia that upregulate CD11c, we generated bone marrow chimeras and found that miR-31 expression was specific to bone marrow-derived DCs (BMDCs). Interestingly, miR-31 binding sites were enriched in mRNAs downregulated BMDCs that migrated into the CNS. Finally, miR-31 was enriched in DCs that migrated through an in vitro blood-brain barrier. Our findings suggest that miRNAs, including miR-31, may participate in the regulation of DCs entry into the CNS during EAE and could potentially represent therapeutic targets for CNS autoimmune diseases such as MS.
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Project description:Background: Previous work has identified CD11c+CD1c- dendritic cells (DCs) as the major 'inflammatory' dermal DC population in psoriasis vulgaris and CD1c+ DCs as the 'resident' cutaneous DC population. Objective: To further define molecular differences between these two myeloid dermal DC populations. Methods: Inflammatory and resident DCs were single-cell sorted from psoriasis lesional skin biopsies, and gene array expression profiling was performed. Results were confirmed with RT-PCR, flow cytometry, immunohistochemistry, and double label immunofluorescence. Pooled human keratinocytes were cultured for functional studies. Results: TNF-related apoptosis-inducing ligand (TRAIL), Toll-like receptors (TLRs) 1 and 2, S100A12/EN-RAGE, CD32, and many other inflammatory products were selectively expressed in inflammatory DCs than in resident DCs. Flow cytometry and immunofluorescence confirmed higher protein expression on CD1c- versus CD1c+ DCs. TRAIL receptor, death receptor 4 (DR4), was expressed on basal keratinocytes and blood vessels, and in vitro culture of keratinocytes with rh-TRAIL induced CCL20 leukocyte chemokine. Conclusion: CD11c+CD1c- inflammatory DCs in psoriatic lesional skin express a wide range of inflammatory molecules compared to skin resident CD1c+ DCs. Some molecules made by inflammatory DCs, including TRAIL, could have direct effects on keratinocytes or other skin cell types to promote disease pathogenesis. Shave biopsies were cultured overnight in dispase to remove the epidermis. Dermis was cultured for 36-48 hours to obtain dermal single cell suspensions. These cells were stained with HLA-DR, CD11c, BDCA-1 (DCs) and FACS-sorted into HLA-DR+11c+BDCA-1+, HLA-DR+11c+BDCA-1- populations into Trizol. RNA was extracted and processed for microarray. 2 dependent groups.
2010-06-08 | E-GEOD-20264 | biostudies-arrayexpress
Project description:Introduction: DCs sense and respond to a variety of pathogen-dependent and independent features. We found that DCs can directly sense the presence of immunological memory in the form of effector memory T cells. This activation by effector memory T cells led to a robust inflammatory signature in interacting DCs. Method: Bone marrow derived DCs (BMDCs) were differentiated in the presence of GMCSF for 7 days. WT naïve T cells were polarized to Th0 (platebound anti-CD3 and anti-CD28 and soluble IL-2) for 5 days, followed by 2 days of rest in low IL-2 containing media to mimic generation of effector memory T cells. CD11c+ BMDCs were sorted via AutoMacs and activated with LPS (100ng/mL) or effector memory T cells (ratio of 1:4) in the presence or absence of soluble anti-CD3 (200ng/mL) for 3 hours. Cells were blocked with FC block and stained with flourophores to distinguish DCs from T cells. DCs were FACS sorted and lysed in Trizol. Conclusion: BMDCs activated with LPS or effector memory T cells had a distict transcriptional response. When activated with effector memory T cells, BMDCs upregulated genes associated with TNFRSF signaling. BMDCs activated with LPS or effector memory T cells also shared certain transcriptional features of upregulated cytokine and chemokine expression.
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Project description:Global gene expression in C. parvum environmental stage (oocysts) and the oocysts treated with UV comparing control untreated ones. Goal was to uncover the metabolic features in oocysts and the oocysts treated with UV.
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Project description:Background: Previous work has identified CD11c+CD1c- dendritic cells (DCs) as the major ”inflammatory” dermal DC population in psoriasis vulgaris and CD1c+ DCs as the “resident” cutaneous DC population. Objective: To further define molecular differences between these two myeloid dermal DC populations. Methods: Inflammatory and resident DCs were single-cell sorted from psoriasis lesional skin biopsies, and gene array expression profiling was performed. Results were confirmed with RT-PCR, flow cytometry, immunohistochemistry, and double label immunofluorescence. Pooled human keratinocytes were cultured for functional studies. Results: TNF-related apoptosis-inducing ligand (TRAIL), Toll-like receptors (TLRs) 1 and 2, S100A12/EN-RAGE, CD32, and many other inflammatory products were selectively expressed in inflammatory DCs than in resident DCs. Flow cytometry and immunofluorescence confirmed higher protein expression on CD1c- versus CD1c+ DCs. TRAIL receptor, death receptor 4 (DR4), was expressed on basal keratinocytes and blood vessels, and in vitro culture of keratinocytes with rh-TRAIL induced CCL20 leukocyte chemokine. Conclusion: CD11c+CD1c- inflammatory DCs in psoriatic lesional skin express a wide range of inflammatory molecules compared to skin resident CD1c+ DCs. Some molecules made by inflammatory DCs, including TRAIL, could have direct effects on keratinocytes or other skin cell types to promote disease pathogenesis.
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Project description:Thymi from Foxn1cre x ROSA26TdTOMATO were enzymaticaly digested, cells were MACS enriched for CD11c+ fraction. Dendritic cells were then FACS sorted (BD influx sorter) as Gr-1-CD11c+TdTOMATO+. TdTOMATO DCs represent fraction of thymic DCs which acquire antigen (TdTOMATO) from thymic epithelial cells, through the process of antigen transfer.
2020-03-20 | E-MTAB-8028 | biostudies-arrayexpress