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The co-exposure responses in the Th2high BN incorporated type I interferon/Th1, alternative macrophage activation/Th2 and Th17 signatures
We employed a systems biology approach to delineate upper airway gene network patterns underlying asthma exacerbation phenotypes in children.
To introduce a disease prognosis framework enabled by a robust classification scheme derived from patient-specific transcriptomic response to stimulation.
CFTR-dependent imbalance of macrophage phenotypes and functions could contribute to the exaggerated inflammatory response seen in CF lung disease
HRV-1B infection directly alters human airway epithelial TJ expression leading to increased epithelial permeability potentially via antiviral response of IL-15
Honorary Research Associate
Alexander Anthony Deborah Pat Larcombe Kicic Strickland Holt BScEnv (Hons) PhD BSc (Hons) PhD PhD PhD, DSc, FRCPath, FRCPI, FAA Honorary Research
High risk for virus-induced asthma exacerbations in children is associated with an IRF7lo immunophenotype, but the underlying mechanisms are unclear. Here, we applied a Systems Biology approach to an animal model comprising rat strains manifesting high versus low susceptibility to experimental asthma, induced by virus/allergen coexposure, to elucidate the mechanism(s)-of-action of the high-risk asthma immunophenotype.
Anaphylaxis is a severe, potentially life-threatening allergic reaction driven primarily by the activation of mast cells. We still fail to understand factors underlying reaction severity. Furthermore, there is currently no reliable diagnostic test to confirm anaphylaxis in the emergency department.
The transcriptome represents the entire set of RNA transcripts expressed in a cell, reflecting both the underlying genetic and epigenetic landscape and environmental influences, providing a comprehensive view of functional cellular states at any given time. Recent technological advances now enable the study of the transcriptome at the resolution of individual cells, providing exciting opportunities to characterise cellular and molecular events that underpin immune-medicated diseases.