Mus musculus
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ABSTRACT:
PROVIDER: PRJNA358682 | ENA |
REPOSITORIES: ENA
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Project description:Visceral leishmaniasis (VL), caused by Leishmania spp protozoan parasites, can provoke overwhelming and protracted epidemics, with high case–fatality rates. Despite extensive efforts towards the development of an effective prophylactic vaccine, no promising vaccine is available yet for humans. Multi-epitope peptide based vaccine development is manifesting as the new era of vaccination strategies against VL. Aim of the study was the design of chimeric peptides from immunogenic L. infantum proteins for encapsulation in PLGA nanoparticles (NPs) alone or in combination with MPLA adjuvant, or in PLGA NPs surface modified with an octapeptide mimicking TNF-alpha for DCs targeting, in order to construct a peptide-based nanovaccine. The in vitro evaluation of the above nanoformulations was performed in DCs isolated from HLA-A2.1 transgenic mice. Characterization of DCs transcriptional responses to these vaccine candidates via microarrays could improve our understanding of their mechanisms of action on DCs' functional differentiation and the type of adaptive immunity subsequently induced.
2016-12-24 | GSE92869 | GEO
Project description:Visceral leishmaniasis (VL) caused by Leishmania donovani and L. infantum is a potentially fatal disease. To date there are no registered vaccines for disease prevention despite the fact that several vaccines are in preclinical development. Thus, new strategies are needed to improve vaccine efficacy based on a better understanding of the mechanisms mediating protective immunity and mechanisms of host immune responses subversion by immunopathogenic components of Leishmania. In the present study, determination of the immune mechanisms related to infection or protective immune responses against VL using an experimental nanovaccine as a vaccine model was conducted through microarray analysis.
2019-11-19 | GSE134661 | GEO
Project description:The mechanisms by which dendritic cells (DCs) induce differentiation of naïve CD4+ T cells along the Th2 lineage is not well understood given that DCs themselves do not produce IL-4. In the present study, we undertook a microarray approach to identify genes involved in the induction of Th2 differentiation by DCs treated with a Th2-skewing adjuvant cholera toxin (CT). In the microarray analysis, murine bone marrow derived immature DCs were treated with CT. Of particular interest was tthe significant upregulation of the expression of c-kit. The upregulation of c-kit on DCs is critical for the induction of a Th2 response. Keywords: cholera toxin, bone marrow derived dendritic cells, gene expression array-based (RNA / spotted DNA/cDNA) Murine bone marrow cells were cultured in the presence of GM-CSF (10 ng/ml) for 6 days . On day 6 the cells were harvested and purified using magnetically labeled anti mouse CD11c+ beads . The DCs were stimulated with CT (1 ug/ml) for 24 hours and the RNA was isolated.
2008-04-14 | E-GEOD-10815 | biostudies-arrayexpress
Project description:Comparison of gene expression in bone marrow-derived dendritic cells (DCs) unstimulated or stimulated with Bifidobacterium in vitro.
2015-11-12 | GSE73476 | GEO
Project description:We aimed to characterize the proteome remodeling in DCs induced upon antigen presentation. To do so, we used an in vitro antigen presentation model to generate postsynaptic (psDC) or nonsynaptic (nsDC) DCs similarly to previously reported (Alcaraz-Serna et al., 2021). Bone marrow-derived DCs (BMDCs), which had been activated with LPS and pulsed (psDC) or not (nsDC) with the ovalbumin peptide OVA323-339, were co-cultured with resting CD4+ T cells from OT-II mice to allow cognate antigen-dependent immune synapse formation (psDC) or not (nsDC). DCs were then purified for proteomic analysis by using mass spectrometry based on multiplexed isotopic labeling peptides approach.
2024-01-26 | PXD039035 | Pride
Project description:Visceral leishmaniasis (VL) is a neglected tropical disease caused by protozoan parasites. An inflammatory immune response, associated with tissue injury, is occurring shortly after infection. In this study, using a rhesus macaque (RMs) model of VL, we evaluated the impact of miltefosine (HePC) therapy administrated during the acute phase of infection. Despite drug therapy, parasites persist in multiple tissues, including the spleen, bone marrow, peripheral (PLN) and mesenteric lymph nodes (MLNs). Parasite burden inversely correlate with cellular HePC levels. Notably, L. infantum remains detectable three months post-treatment. Single-cell transcriptomic analysis reveals significant cellular heterogeneity and reprogramming of splenic myeloid cell populations that persist post-treatment. This included the emergence of inflammatory macrophages, immature plasmacytoid dendritic cells (pDCs), and type 2 dendritic cells (DCs). Flow cytometric sorting of splenic neutrophils, macrophages, and DCs confirms the presence of L. infantum post-treatment, highlighting the challenge of parasite clearance. Collectively, our findings reveal a disrupted innate immune landscape following L. infantum infection that persists after treatment, enlightening myeloid cell reprogramming that may contribute in sustaining chronic infection and parasite persistence.
2025-12-09 | GSE307619 | GEO
Project description:Extracellular vesicles (EVs) include a heterogeneous group of particles. Microvesicles and exosomes are the most characterised vesicles. They can be distinguished by their size, morphology, origin and molecular composition. To date, increasing studies demonstrate that EVs mediates intercellular communication. EVs reach considerable interest in the scientific community due to their role in diverse processes including antigen-presentation, stimulation of anti-tumoral immune responses, tolerogenic or inflammatory effects. In pathogens, EVs shedding is well described in fungus, bacteria, protozoan parasites and helminths. For Trypanosoma cruzi EVs liberation and protein composition was previously described. Dendritic cells (DCs) are key players promoting the immune response against pathogens and also maintaining self-tolerance. In previous reports we have demonstrate that T. cruzi downregulates DCs immunogenicity in vitro and in vivo. Here we analyze EVs from the in vitro interaction between blood circulating tripomastigotes (Tp) and bone-marrow-derived DCs. We found that Tp incremented the number and the size of EVs in cultures with DCs. EVs displayed some exosome markers and intracellular RNA. Protein analysis demonstrated that the parasite changes the protein-EV profile of DCs. We observed that EVs from the interaction of Tp-DCs were easily captured by unstimulated-DCs in comparison with EVs from DCs cultured without the parasite, and also modify the activation status of LPS-stimulated DCs. Noteworthy, we found protection in animal treated with EVs DCs+Tp and challenged with T. cruzi lethal infection. Our goal is to go deep into the molecular characterization of EVs from the DCs-Tp interaction, in order to identify mediators for therapeutic purposes.
2022-11-09 | PXD037795 | Pride
Project description:The goal of this study is to investigate the involvement of inflammation in Alzheimer’s disease (AD) and to clarify the signaling pathways involved in the presence of beta-amyloidosis, a hallmark of AD pathogenesis, to help identifying potential targets for therapy. To do that, we isolated bone marrow-derived progenitor cells from femurs, tibiae and hip bones of non-transgenic C57BL/6 mice according to established protocols , and we maturated them with LPS. To obtain an unbiased view of gene regulation in mouse bone marrow-derived dendritic cells (BM-DCs) exposed to pre-aggregated beta-amyloid peptide (Aβ) oligomers, we analyzed the transcriptome of untreated immature control BM-DCs (‘Ctrl’), LPS-treated BM-DCs (’LPS’), Aβ1-42 oligomer-treated BM-DCs (‘Aβ‘) and BM-DCs treated with Aβ1-42 oligomers and LPS (‘Aβ+LPS‘) via explorative RNA-sequencing.
2019-09-16 | GSE136789 | GEO
Project description:Infection of mouse bone marrow Flts3L-derived dendritic cells (FL-DCs) with chimeric human T cell leukemia virus type 1 (HTLV-1) results in the upregulation as well as selective downregulation of various interferon-stimulated genes. Mouse bone marrow Flt3L-derived dendritic cells were infected with chimeric HTLV-1 and analyzed for the expression of type 1 interferon-stimulated genes after 4 hours. The expression of various genes was compared to the control (non-infected) cells.
2010-10-28 | E-GEOD-24957 | biostudies-arrayexpress
Project description:Infection of mouse bone marrow Flts3L-derived dendritic cells (FL-DCs) with chimeric human T cell leukemia virus type 1 (HTLV-1) results in the upregulation as well as selective downregulation of various interferon-stimulated genes.
2010-10-28 | GSE24957 | GEO