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3,441 results for “Immune cells”
Integrative analyses of single-cell transcriptome and immune profiling reveal clonal expansion of T cells in the blood and cerebrospinal fluid of Parkinson's disease
<p>An increasing number of studies has indicated that the immune system plays important roles in the pathogenesis of Parkinson's disease. However, little is known about the contribution of adaptive immune responses in Parkinson's disease. Here, we performed comprehensive integrative analyses of single-cell transcriptome and immune profiling of the blood of 8 Parkinson's patients and 13 healthy controls as well as the cerebrospinal fluid of 6 Parkinson's patients, 4 Alzheimer's patients, 5 mild cognitive impairment (MCI) patients and 9 healthy controls. In total, 22 T cell subsets with distinct functions and clonalities were identified from 121,402 T cells. We observed significant clonal expansion of effector CD8+ T cells in Parkinson's patients, which formed a gradient of transcriptional states from central memory CD8+ T cells to early effector CD8+ T cells followed by terminal effector CD8+ T cells. Shared TCRs in this progression suggest TCRs may be involved in the state transition of CD8+ T cells stimulated by antigens. Notably, we also found that a group of clonally expanded cytotoxic CD4+ T cells were significantly increased in Parkinson's patients compared to controls, suggesting their cytotoxic roles in Parkinson's disease. Finally, we screened putative TCR-antigen pairs that existed in both blood and cerebrospinal fluid of patients with Parkinson's disease. These results reveal an adaptive immune response in the blood and cerebrospinal fluid of Parkinson's disease and provide novel evidence of clonal, antigen-experienced T cells patrolling in the blood and cerebrospinal fluid of Parkinson's disease.</p>
Data from: A single 17D Yellow Fever vaccination provides lifelong immunity; characterization of Yellow-Fever-specific neutralizing antibody and T-cell responses after vaccination
Introduction: Prompted by recent amendments of Yellow Fever (YF) vaccination guidelines from boost to single vaccination strategy and the paucity of clinical data to support this adjustment, we used the profile of the YF-specific CD8+ T-cell subset profiles after primary vaccination and neutralizing antibodies as a proxy for potentially longer lasting immunity. Methods and Findings: PBMCs and serum were collected in six individuals on days 0, 3, 5, 12, 28 and 180, and in 99 individuals >10 years after YF-vaccination. Phenotypic characteristics of YF- tetramer+ CD8+ T-cells were determined using class I tetramers. Antibody responses were measured using a standardized plaque reduction neutralization test (PRNT). Also, characteristics of YF-tetramer positive CD8+ T-cells were compared between individuals who had received a primary- and a booster vaccination. YF-tetramer+ CD8+ T-cells were detectable on day 12 (median tetramer+ cells as percentage of CD8+ T-cells 0.2%, range 0.07–3.1%). On day 180, these cells were still present (median 0.06%, range 0.02–0.78%). The phenotype of YF-tetramer positive CD8+ T-cells shifted from acute phase effector cells on day 12, to late differentiated or effector memory phenotype (CD45RA-/+CD27-) on day 28. Two subsets of YF-tetramer positive T-cells (CD45RA+CD27- and CD45RA+CD27+) persisted until day 180. Within all phenotypic subsets, the T-bet: Eomes ratio tended to be high on day 28 after vaccination and shifted towards predominant Eomes expression on day 180 (median 6.0 (day 28) vs. 2.2 (day 180) p = 0.0625), suggestive of imprinting compatible with long-lived memory properties. YF-tetramer positive CD8+ T-cells were detectable up to 18 years post vaccination, YF-specific antibodies were detectable up to 40 years after single vaccination. Booster vaccination did not increase titers of YF-specific antibodies (mean 12.5 vs. 13.1, p = 0.583), nor induce frequencies or alter phenotypes of YF-tetramer+ CD8+ T-cells. Conclusion: The presence of a functionally competent YF-specific memory T-cell pool 18 years and sufficient titers of neutralizing antibodies 35–40 years after first vaccination suggest that single vaccination may be sufficient to provide long-term immunity.
Data from: Down syndrome cell adhesion molecule 1: testing for a role in insect immunity, behaviour and reproduction
Down syndrome cell adhesion molecule 1 (Dscam1) has wide-reaching and vital neuronal functions although the role it plays in insect and crustacean immunity is less well understood. In this study, we combine different approaches to understand the roles that Dscam1 plays in fitness-related contexts in two model insect species. Contrary to our expectations, we found no short-term modulation of Dscam1 gene expression after haemocoelic or oral bacterial exposure in Tribolium castaneum, or after haemocoelic bacterial exposure in Drosophila melanogaster. Furthermore, RNAi-mediated Dscam1 knockdown and subsequent bacterial exposure did not reduce T. castaneum survival. However, Dscam1 knockdown in larvae resulted in adult locomotion defects, as well as dramatically reduced fecundity in males and females. We suggest that Dscam1 does not always play a straightforward role in immunity, but strongly influences behaviour and fecundity. This study takes a step towards understanding more about the role of this intriguing gene from different phenotypic perspectives.
Machine Learning-assisted immunophenotyping of peripheral blood identifies innate immune cells as best predictor of response to induction chemo-immunotherapy in head and neck squamous cell carcinoma – knowledge obtained from the CheckRad-CD8 trial
<p>Raw cell counts from peripheral blood immune phenotyping across individual patients.</p>
Single cell RNA-seq transcriptomic profile of circulating immune and progenitor cells in a mouse model of neonatal hypoxic/ischemic (HI) brain damage.
<p>Hematopoietic cells play a pivotal role in regulating the inflammatory and reparative immune responses triggered after ischemic tissue damage. The response initiated within the injured tissue leads to compositional and transcriptional changes in circulating hematopoietic and progenitor cells, which have been utilized as biomarkers. While the importance of different immune and progenitor cell subtypes in the development of ischemic damage has been extensively researched in adult tissue injuries, there has been limited investigation in neonates. This is a critical developmental stage where ischemic damage can result in severe and irreversible health consequences if not promptly treated. To determine how ischemic damage could affect circulating cells in neonates, we have induced hypoxic-ischemic (HI) brain damage in seven-day-old mice, characterized by focal white and gray-matter injury (Rice-Vannucci model). Brain damage and circulating cells were analyzed at 48h post-HI, the intermediate reparative/inflammatory response phase post-injury. We applied scRNAseq to dissect the transcriptional and cellular composition changes in the peripheral blood of HI-treated and SHAM control neonates. This study provides the first scRNAseq dataset for immune and progenitor circulating cells in newborns with cerebral HI damage. It may help to identify biomarkers and selective therapeutic approaches aimed at modulating inflammatory and reparative pathways. </p><p>CD1 postnatal day 7 (P7) mice were subjected to hypoxic/ischemic (HI) brain injury by permanent ligation of the left common carotid artery followed, after 2h recover, by relocation to a hypoxia chamber for 90 minutes. Sham control mice (SHAM) underwent a skin incision and wound closure followed by hypoxia exposure. Circulating blood cells were collected from SHAM and HI mice at P9. After red blood cells (RBC) lysis, 7AAD-Ter119- cells were FACS sorted and analysed using sc RNAseq. Other samples were FACS sorted for CD45+CD11+ and CD45-CD31+ cells and mixed.</p>
Immune cell parameters found to be impacted in patients with autoimmune and autoinflammatory disorders enrolled in the Transimmunom study.
<p>Expanding upon the Transimmunom clinical trial, we gathered peripheral blood samples from 443 patients enrolled between 2015 and 2022, who were afflicted with 15 distinct autoimmune or autoinflammatory diseases or related conditions. Additionally, blood samples were collected from 71 healthy volunteers to establish a reference condition. The screened disorders spanned a spectrum from purely autoinflammatory to purely autoimmune diseases, encompassing various levels of disorder activities without a specific threshold. The disorders examined included arthritis conditions such as Behçet's disease (BD; n=38), knee osteoarthritis (OA; n=45), rheumatoid arthritis (RA; n=91), spondylarthritis (SA; n=58), and systemic lupus erythematosus (SLE; n=33). Blood vessel disorders, such as Antiphospholipid syndrome (APLS; n=23), Churg-Strauss's disease (CS; n=6), Granulomatosis with polyangiitis (GPA; n=14), and Takayasu arteritis (TA; n=22), were also included. Metabolic disorders like Type 1 Diabetes (T1D; n=60) and Type 2 Diabetes (T2D; n=27), muscle disorder (Myositis; n=4), inflammatory bowel diseases (IBD) like Crohn's disease (CD; n=10) and ulcerative colitis (UC; n=5), as well as IBD-like diseases including Familial Mediterranean Fever (FMF; n=7), were part of the study.</p><p>To analyze the patient blood samples, we utilized 12 flow cytometry panels, each consisting of 10 cell markers. We introduced an extra panel specifically designed to identify the primary immune cell populations. This panel featured numeration beads, enabling the determination of absolute counts for all populations. It served as a reference tube, facilitating the calculation of absolute counts in all other panels through extrapolation from shared populations. In total, we analyzed more than 600 innate and adaptive immune cell parameters (both absolute cell counts and percentages) from patient's blood.</p><p>The provided data encompasses significant flow cytometry data related to the Transimmunom study. This dataset specifically details the values of 224 cell parameters that exhibit significant differential abundance in at least one disease when compared to samples from healthy volunteers. Both Cliff's Delta effect size and two-way non-parametric Wilcoxon test were used to identify cell parameters significantly differentially abundant between conditions. Cell parameters with an absolute value of Cliff's Delta effect size higher than 0.33 and with a p-value lower than 0.05 were considered statistically significant. </p><p>The provided file is formatted as a tab-separated file. Each row corresponds to a specific cell parameter, either representing cell percentage or absolute cell count. Each column corresponds to a distinct patient, identified by the disease name and anonymous identifier.</p>
OrganoIDNetData: A Curated Cell Life Imaging Dataset of Immune-enriched Pancreatic Cancer Organoids with Pre-trained AI Models
<p>OrganoIDNetData encompasses 180 images with 34113 organoids of human and murine Pancreatic Ductal Adenocarcinoma co-cultured with immune cells.</p> <p><strong>For further information and to cite this dataset, please refer to:</strong></p> <p>Kulkarni, A., Ferreira, N., Scodellaro, R. <em>et al.</em> A Curated Cell Life Imaging Dataset of Immune-enriched Pancreatic Cancer Organoids with Pre-trained AI Models. <em>Sci Data</em> <strong>11</strong>, 820 (2024). https://doi.org/10.1038/s41597-024-03631-3</p>
Learning the sequence code for protein abundance in human immune cells
<p><span>Protein abundance is defined by </span><span>transcriptional, post-transcriptional and post-translational regulatory mechanisms. Understanding the code for gene expression could inform novel therapies. Here, we developed a machine learning pipeline, termed SONAR, to decipher the endogenous sequence code that defines the abundance of protein in human cells. SONAR predicts up to 63% of protein abundance independently of promoter or enhancer information. Our analysis reveals a strong - yet dynamic - </span><span>cell-type specific sequence code<span>. The deep knowledge of SONAR provides a map of biologically active sequence features (SFs), which we leveraged to </span></span><span>manipulate protein expression and tailored to a specific cell-type. </span><span>Beyond providing fundamental insights in gene expression regulation, our study offers novel means to improve therapeutic and biotechnology applications.</span></p> <p><span>Datasets of the protein models (with gamma=1) are included in this repository. Please refer to GitHub for more details on how the models were generated. </span></p>
Infection of HSV1 in innate lymphoid cells leads to alienation of the mechanism of T/B-cell activation in the adaptive immune response-image
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raw data - Causal relationship of immune cells and primary open-angle glaucoma: A Mendelian randomization study
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Brood sex ratio, early chick survival, and cell-mediated immunity measurements for 3 experimental groups of Larus canus and Chroicocephalus ridibundus pairs
<p>Sex allocation theory predicts that parents should adjust their brood sex ratio to maximize fitness returns in relation to parental investment. Adaptive adjustment of sex ratio may be driven by differential costs of rearing sons and daughters or differential benefits of investing limited resources into offspring of different sex. In both cases, possible sex ratio bias should depend on parental condition. For sexually dimorphic birds with males larger than females, sons may be less likely to fledge since they are more vulnerable to food shortages or because they have impaired immunocompetence due to higher testosterone levels. Poor condition females should thus overproduce daughters to minimize possible reproductive failure. We manipulated the number of eggs laid and the amount of food available to laying females to induce differences in the condition in two gull species differing in sexual size-dimorphism. In the Black-headed Gull (<em>Chroicocephalus ridibundus</em>), sexual size differences are marginal, but in the Mew Gull (Larus canus, MG) males are 11% larger. In both species, females forced to lay an additional egg (presumed in worse condition) overproduced daughters, while females receiving supplemental food before laying (presumed improved condition) overproduced sons. This sex ratio skew was larger in MG, species with larger size dimorphism. Chick immunocompetence at hatching was unrelated to sex, being higher in broods of fed mothers and lower for chicks hatched from last-laid eggs. Chick survival between hatching and day 5 post-hatch was positively related to their immunocompetence, but chicks from last-laid eggs and males of the more dimorphic species (MG) survived less well. Results indicate that costs of raising larger sex offspring coupled with parental condition shape brood sex ratio in populations studied. Adaptive brood sex ratio adjustment occurs mostly before egg-laying and includes differential sex allocation in eggs depending on the probability of producing a fledged chick.</p>
Altered Frequencies and Functions of Innate Lymphoid Cells in Melanoma Patients Are Modulated by Immune Checkpoints Inhibitors
<p>Raw data related to limphocytes subpopulation.</p> <p>This work was supported by Italian Association for Cancer Research (IG15521 and IG20312); Wenner-Gren Foundation, Sweden; Fondazione Melanoma Onlus, Naples; Ministero dell’Istruzione, dell’Università e della Ricerca (MIUR) PRIN 2017 2017M8YMR8_002; Fondazione NIBIT, Siena, Italy (grants to EC) and Italian Ministry of Health (IT-MOH) through “Ricerca Corrente”, grants number M2-2 (grants to PAA). CMC was supported by EFIS-IL Short Term Fellowship and EACR Travel Fellowship.</p> <p> </p> <p> </p>
Avian auditory hair cell regeneration is accompanied by JAK/STAT-dependent expression of immune-related genes in supporting cells
<p>Normalized log count matrix and single cell experiment container</p>
Human adipose-derived mesenchymal stem cells prevent type 1 diabetes induced by immune checkpoint blockade
<p class="MsoNormal"><span><strong>Aims/hypothesis</strong></span></p> <p class="MsoNormal"><span> Immunomodulators blocking cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) or programmed death-ligand 1 (PD-L1) have improved the treatment of a broad spectrum of cancers. These immune checkpoint inhibitors (ICIs) reactivate the immune system against tumour cells but can also trigger autoimmune side effects, including type 1 diabetes. Mesenchymal stem cell (MSC) therapy is the most prevalent cell therapy, with tissue-regenerating, anti-fibrosis and immunomodulatory functions provided by the secretome of the cells. Here, we examined whether systemic MSC treatment could prevent the development of type 1 diabetes in a NOD mouse model.</span></p> <p class="MsoNormal"><span><strong>Methods</strong> </span></p> <p class="MsoNormal"><span>The purified PD-L1 monoclonal antibody was administered to induce diabetes in male NOD mice which normally do not develop diabetes. Human adipose-derived MSCs were administered by tail vein injections. T cells, macrophages and monocyte-derived macrophages expressing C-X-C motif chemokine ligand 9 (CXCL9) in pancreatic sections of NOD mice and a cancer patient who developed diabetes following the ICI treatments were analysed by immunofluorescence. Tissue localisation of the injected MSCs, plasma exosome levels and plasma cytokine profiles were also investigated.</span></p> <p class="MsoNormal"><span><strong>Results</strong> </span></p> <p class="MsoNormal"><span>PD-1/PD-L1 blockade induced diabetes in 16 of 25 (64%) NOD mice which received anti-PD-L1 mAb without hMSCs [MSC(−)], whereas MSC administration decreased the incidence to four of 21 (19%) NOD mice which received anti-PD-L1 mAb and hMSCs [MSC(+)]. The PD-1/PD-L1 blockade significantly increased the area of CD3-positive T cells (6.2-fold) and Macrophage-2 (Mac-2) antigen (2.5-fold)- and CXCL9 (40.3-fold)-positive macrophages in the islets. MSCs significantly reduced T cell (45%) and CXCL9-positive macrophage (67%) accumulation in the islets and the occurrence of diabetes. The insulin content (1.9-fold) and islet beta cell area (2.7-fold) were also improved by MSCs. T cells and CXCL9-positive macrophages infiltrated into the intricate gaps between the beta cells in the islets by PD-1/PD-L1 blockade. Such immune cell infiltration was largely prevented by MSCs. The most striking difference was observed in the CXCL9-positive macrophages, which normally did not reside in the beta cell region in the islets but abundantly accumulated in this area after PD-1/PD-L1 blockade and were prevented by MSCs. The CXCL9-positive macrophages were also observed in the islets of a cancer patient who developed diabetes following the administration of ICIs but little was observed in a control patient. Mechanistically, the injected MSCs accumulated in the lung but not in the pancreas and strongly increased plasma exosome levels and changed plasma cytokine profiles.</span></p> <p class="MsoNormal"><span><strong>Conclusions/interpretation</strong></span></p> <p class="MsoNormal"><span> Our results suggest that MSCs can prevent the incidence of diabetes associated with immune checkpoint cancer therapy and may be worth further consideration for new adjuvant cell therapy.</span></p> <p class="MsoNormal"><span><strong>Data availability</strong> </span></p> <p class="MsoNormal"><span>All datasets were deposited to DOI https://doi.org/10.5061/dryad.xwdbrv1fh.</span></p>
Spatial distribution pattern of immune cells is associated with patient prognosis in colorectal cancer
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Blockade of LAG3 and PD1 leads to co-expression of cytotoxic and exhaustion gene modules in CD8+ T cells to promote antitumor immunity
<p>This is the data necessary to reproduce the figures from "<em>Blockade of LAG3 and PD1 leads to co-expression of cytotoxic and exhaustion gene modules in CD8+ T cells to promote antitumor immunity</em>" by Cillo et al.</p>
Data from: Identification and validation of a novel immune-related signature associated with macrophages and CD8 T cell infiltration predicting overall survival for hepatocellular carcinoma
<p><b>Background:</b> Although the effects of macrophages and CD8 T cell infiltration on clinical outcomes have been widely reported, the association between immunity-associated gene with them for hepatocellular carcinoma (HCC) remains unclear.</p> <p><b>Materials and methods: </b>The ssGSEA served for quantifying the macrophages as well as CD8 T cell infiltration in the HCC samples obtained from TCGA database. Kaplan-Meier(KM) survival assay was used to determine the associations between macrophages and CD8 T cell infiltration with OS. LASSO Cox regressive method assisted in developing an immune gene signature as well as building a risk score. The performance was evaluated by the time-dependent ROC together with the KM survival analysis. The ICGC database were adopted for external verification. CIBERSORT was applied to the correlation analysis on the immune-related signature and the immunocyte infiltration. GSEA were employed exploring the underlying molecular mechanisms.</p> <p><b>Results:</b> Increased CD8+ T cell infiltration was associated with longer OS, whereas a greater infiltration of macrophages was related to shorter OS. There were 398 differential expression genes (DEGs) between the high- and low infiltration groups with the "edgeR" package. A prognostic signature consisted of 10 immune genes was built in TCGA and examined in ICGC. The uniform cutoff (0.927) was adopted for separating sufferers into the high-risk(HR) and low-risk(LR) groups. The ROC curves revealed that the AUC data for this signature predicting 1,2,3,4 and 5 year were all above 0.7 in both TCGA and ICGC cohort and patients in the HR<sub> </sub>group exhibited evidently weaker prognostic results compared with the LR group. The HR<sub> </sub>group presented evidently greater Tregs and Macrophage M0 relative to the LR group, whereas the LR group saw the enrichment of CD8 T cells.</p> <p><b>Conclusion:</b> The immune signature associated with macrophages as well as CD8 T cell infiltration has reliable prognostic and predictive value for HCC patients.</p>
Raw Data for the article: Human Amnion-Derived Mesenchymal Stromal/Stem Cells Pre-Conditioning Inhibits Inflammation and Apoptosis of Immune and Parenchymal Cells in an In Vitro Model of Liver Ischemia/Reperfusion
<p>Ischemia/reperfusion injury (IRI) represents one of the leading causes of primary non-function acute liver transplantation failure. IRI, generated by an interruption of organ blood flow and the subsequent restoration upon transplant, i.e., reperfusion, generates the activation of an inflammatory cascade from the resident Kupffer cells, leading first to neutrophils recruitment and second to apoptosis of the parenchyma. Recently, human mesenchymal stromal/stem cells (hMSCs) and derivatives have been implemented for reducing the damage induced by IRI. Interestingly, sparse data in the literature have described the use of human amnion-derived MSCs (hAMSCs) and, more importantly, no evidence regarding hMSCs priming on liver IRI have been described yet. Thus, our study focused on the definition of an in vitro model of liver IRI to test the effect of primed hAMSCs to reduce IRI damage on immune and hepatic cells. We found that the IFNγ pre-treatment and 3D culture of hAMSCs strongly reduced inflammation induced by M1-differentiated macrophages. Furthermore, primed hAMSCs significantly inhibited parenchymal apoptosis at early timepoints of reperfusion by blocking the activation of caspase 3/7. All together, these data demonstrate that hAMSCs priming significantly overcomes IRI effects in vitro by engaging the possibility of defining the molecular pathways involved in this process.</p>
Study of Vitespen (HSPPC-96, Oncophage ®) for Immune Response Assessment in Participants With Resectable Renal Cell Carcinoma at Intermediate Risk of Recurrence
ClinicalTrials.gov study NCT01147536. IPD Sharing: Not stated. Countries: 2. Publications: 0.
High-throughput Omic Technology for Identification of Biomarkers of Relapsing Acute Disseminated Encephalomyelitis in Immune Cell Network
ClinicalTrials.gov study NCT06863974. IPD Sharing: YES. Countries: 1. Publications: 0.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.