James Read
Honorary Research Associate
james.read@telethonkids.org.au
James received his Bachelor’s from the University of Western Australia with majors in Physiology and Cell Biology in 2012. He then completed his honours in Microbiology at The Marshall Centre, UWA in 2013.
James joined the Cell Biology team at The Kids Research Institute Australia in 2014, working across projects focussed on the understanding of the immunological mechanisms of asthma. In 2017 James began a PhD with the Systems Immunology group through UWA.
His research employs a multi-omics approach to investigate how early life immune responses contribute towards asthma inception and trajectory.
Projects
An immunometabolomic approach to unmask developmental regulation of innate immunity and asthma risk
Published research
Single cell transcriptomics reveals cell type specific features of developmentally regulated responses to lipopolysaccharide between birth and 5 years
Human perinatal life is characterized by a period of extraordinary change during which newborns encounter abundant environmental stimuli and exposure to potential pathogens. To meet such challenges, the neonatal immune system is equipped with unique functional characteristics that adapt to changing conditions as development progresses across the early years of life, but the molecular characteristics of such adaptations remain poorly understood.
Lipopolysaccharide-induced interferon response networks at birth are predictive of severe viral lower respiratory infections in the first year of life
Appropriate innate immune function is essential to limit pathogenesis and severity of severe lower respiratory infections (sLRI) during infancy, a leading cause of hospitalization and risk factor for subsequent asthma in this age group.
Protection against severe infant lower respiratory tract infections by immune training: Mechanistic studies
Results from recent clinical studies suggest potential efficacy of immune training (IT)-based approaches for protection against severe lower respiratory tract infections in infants, but underlying mechanisms are unclear.
Decoding Susceptibility to Respiratory Viral Infections and Asthma Inception in Children
Human Respiratory Syncytial Virus and Human Rhinovirus are the most frequent cause of respiratory tract infections in infants and children and are major triggers of acute viral bronchiolitis, wheezing and asthma exacerbations.
Immunoinflammatory responses to febrile lower respiratory infections in infants display uniquely complex/intense transcriptomic profiles
the association between infant LRTI and risk for persistent wheeze/asthma in this cohort is generally stronger for fLRTIs than for other infection categories
Progressive increase of FcεRI expression across several PBMC subsets is associated with atopy and atopic asthma within school-aged children
The expression pattern of FcεRI on DC and basophils differentiates asthmatic from non-asthmatic atopic children
Personalized transcriptomics reveals heterogeneous immunophenotypes in children with viral bronchiolitis
Dysregulated expression of IFN-dependent pathways after respiratory viral infections is a defining immunophenotypic feature of AVB-susceptible infants
Upper Airway Cell Transcriptomics Identify a Major New Immunological Phenotype with Strong Clinical Correlates in Young Children with Acute Wheezing
Asthma exacerbations in children can be divided into IRF7hi versus IRF7lo phenotypes with associated differences in clinical phenotypes
CD8+XCR1neg Dendritic Cells Express High Levels of Toll-Like Receptor 5 and a Unique Complement of Endocytic Receptors
Our data demonstrate that CD8+XCR1neg DCs possess a unique pattern of endocytic receptors and a restricted TLR profile that is particularly enriched for TLR5