Julian Charles Knight

This paper introduces scTAPAS, a method to reconstruct donor genotypes from scRNA-seq data, enabling eQTL and HLA-TCR analysis without conventional genotyping.

The paper identifies four genome-wide significant loci affecting monocyte cytokine release and links genetic variants to cytokine secretion patterns.

The paper maps cis- and trans-eQTLs in blood samples to infer gene regulatory networks and prioritize trait-relevant pathways.

The paper identifies structural differences in TCR recognition of the same pMHC ligand using cryo-EM, showing how similar β chains can pair with different α chains to produce distinct recognition modes.

The paper identifies USP18 as a negative regulator of interferon response at a lupus risk locus through trans-eQTL analysis in lymphoblastoid cell lines.

This study analyzes cfDNA in sepsis patients, finding increased levels due to impaired liver clearance rather than immune cell death, and identifies liver and megakaryocyte-erythroid progenitor contributions.

The paper identifies disease-specific genetic regulation of gene expression in immune cells during COVID-19 infection using single-cell eQTL mapping.

The paper tracks T cell responses over time in the tuberculin skin test to identify Mtb-reactive T cell metaclones that are immunodominant across individuals.

Castanet is a pipeline for analyzing multi-pathogen enrichment sequencing data, providing accurate consensus sequences and metrics for pathogen detection and quantification.

This study investigates the genetic and phenotypic associations between endometriosis and 31 immunological diseases using UK Biobank data, finding significant genetic correlations and a causal link with rheumatoid arthritis.

The paper characterizes genetic determinants of context-specific DNA methylation in primary monocytes exposed to inflammatory stimuli, identifying 209 CpGs under genetic control and linking them to disease.

The paper identifies eQTL specific to NK cells and links them to autoimmunity through transcriptome-wide association studies.

The paper identifies deleterious neutrophil states and altered granulopoiesis in sepsis using single-cell multi-omics data from sepsis patients and controls.

The paper investigates how genetic variants associated with ankylosing spondylitis affect c-MYC binding and chromosomal looping near the RUNX3 promoter.

The paper uses blood eQTL meta-analysis to explore the polygenic architecture of complex traits, finding that trans-eQTLs are more informative for identifying causal genes than cis-eQTLs.

The paper uses long-read sequencing and de novo assembly to identify structural variation in immune system gene regions from a single individual, revealing challenges in current variant calling methods.

The paper investigates how a polymorphism in a RUNX3 enhancer affects TF binding in CD8+ T-cells, linking it to ankylosing spondylitis risk.

This study identifies 5,106 new genetic variants associated with blood cell traits using large-scale GWAS, highlighting the polygenic and monogenic basis of hematopoiesis.

This study performs GWAS on blood cell flow-cytometry phenotypes, identifies variant-trait associations, and links them to cellular structures and disease mechanisms.

The paper identifies an association between the HLA-DQA1*01:03 allele and increased risk of invasive group A streptococcal disease using case-control studies and HLA imputation.

The paper uses genome-wide association studies to show human and pneumococcal genetic variation influences susceptibility and severity of pneumococcal meningitis.

The paper investigates how a genetic variant affects IL7R expression and soluble receptor secretion in monocytes under inflammatory conditions.

The paper develops gene-expression-based prognostic models for 30-day mortality in sepsis using community-onset and hospital-acquired sepsis cohorts, showing improved prediction when combined with clinical scores.