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• High titers and low fucosylation of early phase anti-SARS-CoV-2 IgG promote hyper-inflammation by alveolar macrophages

  We show that early phase anti-Spike IgG in serum of critically ill COVID-19 patients induces hyper-inflammatory responses by human alveolar macrophages. We identified that this excessive inflammatory response is dependent on two antibody features that are specific for severe COVID-19. First, inflammation is driven by high titers of anti-Spike IgG, a hallmark of severe disease. Second, we found that anti-Spike IgG from severely ill patients is intrinsically more pro-inflammatory because of different glycosylation of the Fc tail, particularly by low fucosylation. This dataset is linked with the following ArrayExpress Experiment: E-MTAB-10431 - 2020_COVID19_FCGR_MIL10_IgGfucosylation

  Study EGAS00001005206

• A Dose Escalation Study of Efmarodocokin Alfa (UTTR1147A) in Healthy Volunteers and Patients with Ulcerative Colitis

  Background: The interleukin-22 cytokine (IL-22) has demonstrated efficacy in nonclinical colitis models with a non-immunosuppressive mechanism-of-action. Efmarodocokin alfa (UTTR1147A) is a fusion protein agonist that links IL-22 to the crystallizable fragment (Fc) of human immunoglobulin (IgG4) for improved pharmacokinetic characteristics, but with a mutation to minimize Fc effector functions. Methods: This randomized, phase 1b study evaluated the safety, tolerability, pharmacokinetics, and pharmacodynamics of repeat intravenous dosing of efmarodocokin alfa in healthy volunteers (HVs; n=32) and patients with ulcerative colitis (UC; n=24) at 30–90 µg/kg doses given biweekly (Q2W) or monthly (Q4W) (6:2 active:placebo per cohort). Results: The most common adverse events (AEs) were on-target dermatological effects (dry skin, erythema, and pruritus) that were reversible. Dose-limiting non-serious dermatological AEs (severe dry skin, erythema, exfoliation, and discomfort) were seen in two HVs and one patient at 90 ug/kg Q2W. Pharmacokinetics were generally dose-proportional across the dose levels tested, but patients demonstrated lower drug exposures relative to HVs at the same dose. IL-22 serum biomarkers and IL-22 responsive genes in colon biopsies were induced with active treatment. Patients demonstrated changes in microbiota composition following active treatment, thereby reversing baseline dysbiosis. Clinical response was observed in 7/18 active- and 1/6 placebo-treated patients; clinical remission was observed in 5/18 active- and 0/6 placebo-treated patients.

  Study EGAS00001006172

• Ribo-depleted RNA-sequencing of II.3, III.1, and III.3

  This datasets contains the Ribo-depleted RNA-sequencing of patients II.3, III.1, and III.3. Libraries were sequenced to a minimum depth of 195 million read pairs (2x75nts) on an Illumina NextSeq500 Midoutput FC.

  Dataset EGAD50000002364

• Characterizing the cell-free transcriptome in a humanized DLBCL patient-derived tumor xenograft model for RNA-based liquid biopsy in a preclinical setting

  This study explores the cell-free transcriptome in a humanized DLBCL patient-derived tumor xenograft (PDTX) model. Blood plasma samples (n=171) derived from a DLBCL PDTX model including 27 humanized (HIS) PDTX, 8 HIS non-PDTX and 21 non-HIS PDTX NOD-scid IL2Rgnull mice were collected during humanization, xenografting, treatment, and sacrifice. The mice were treated with either R-CHOP, huCD20-Fc-AFN-CHOP, or phosphate-buffered saline (PBS). RNA was extracted using the miRNeasy serum/plasma kit and sequenced on the NovaSeq 6000 platform using the SMARTer Stranded Total RNA-seq pico v3 kit.

  Study EGAS50000000566

• Oral Immunotherapy for Induction of Tolerance and Desensitization in Peanut-Allergic Children (IMPACT)

  Brief Summary:This is a randomized, double-blind, placebo-controlled, multi-center study comparing peanut oral immunotherapy (OIT) to placebo in the induction of tolerance and desensitization in peanut-allergic children. Eligible participants with peanut allergy will be randomly assigned to receive either peanut OIT or placebo for 134 weeks followed by peanut avoidance for 26 weeks.Detailed Description:An initial oral food challenge (OFC) to 1 g of peanut flour (500 mg peanut protein) will be conducted. Participants must have a clinical reaction during this OFC to initiate study dosing. After the initial OFC, the study design includes four phases:Initial dose escalation (1 day): Peanut or placebo dosing will be given incrementally and increase every 20 minutes until a dose of 12 mg peanut flour (6 mg peanut protein) or placebo flour is given. Build-up (30 weeks): Initial observed dose administration of highest tolerated dose, followed by daily OIT at home with return visit every 2 weeks for dose escalation. Maintenance (104 weeks):The participant will continue on daily OIT with return visits every 13 weeks. At the end of this phase the participant will undergo a blinded OFC to 10 g peanut flour (5 g peanut protein). Avoidance (26 weeks): In this final phase participants will be seen every 13 weeks. At the completion of this phase participants will have a final blinded OFC to 10g peanut flour (5 g peanut protein)

  Study phs003109

• H3Africa H3AChipDesign TrypanoGEN1

  26 samples from Cameroon generated for the H3Africa Chip Design Study. The dataset includes BAM, FASTQ and decompressed gVCF files.

  Dataset EGAD00001004393

• dataset1

  Contains test sample 1-26

  Dataset EGAD00010002041

• ATAC-seq

  ATAC-seq data for 26 CLL samples (7 controls, 19 tumor) of the CancerEpiSys-PRECiSe project.

  Dataset EGAD00001005967

• Defining Cutaneous Gene Expression Signatures in Juvenile Dermatomyositis

  Skin inflammation in juvenile dermatomyositis (JDM) can signal disease onset or flare up and prevent complete disease remission. Our objective was to evaluate JDM cutaneous expression signatures through tape stripping in both lesional and non-lesional skin and as compared to paired blood. A total of 28 JDM and 20 control (CTL) patients participated in the study. All patients had tape strip sampling of non-lesional (NL) skin at enrollment visit. Within our JDM cohort, paired lesional (L) skin was additionally sampled if rash was present. 16/28 of JDM patients had at least one additional skin sample associated with a follow-up (FU) visit (total number of follow-up samples included = 26 NL and 4 L). We identified a common innate immune signature in both lesional and non-lesional JDM skin. Using unsupervised hierarchical clustering of skin expression data, we distinguished a JDM molecular subgroup characterized by a mitochondrial dysfunction signature. In comparison to blood expression data, we determined that skin may more effectively highlight the JDM subgroup characterized by a mitochondrial dysfunction expression signature. Data available include bulk RNA-sequencing data from tape strips and blood of the JDM and control patients from this study.

  Study phs003884

• BLUEPRINT release August 2015, ChIP-Seq for CD8-positive, alpha-beta T cell, on genome GRCh38

  ChIP-Seq data for 5 CD8-positive, alpha-beta T cell sample(s). 26 run(s), 26 experiment(s), 26 alignment(s) on human genome GRCh38. Part of BLUEPRINT release August 2015. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20150820/homo_sapiens/README_chipseq_analysis_ebi_20150820

  Dataset EGAD00001001513