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Researchers may have found key to preventing asthma

Researchers have made a world-first discovery on how to prevent severe respiratory infections in babies.

Airway Epithelial Cells Condition Dendritic Cells to Express Multiple Immune Surveillance Genes

AEC-conditioned DC showed selective upregulation of chemokines that recruit Th1 cells, but minimal change in chemokines linked to Th2 cell recruitment.

Interferon regulatory factor 7 is a major hub connecting interferon-mediated responses in virus-induced asthma exacerbations in vivo

The objective of this study was to elucidate the molecular networks that underpin virus-induced exacerbations in asthmatic children in vivo.

Interferon regulatory factor 7 is a major hub connecting interferon-mediated responses in virus-induced asthma exacerbations in vivo

The objective of this study was to elucidate the molecular networks that underpin virus-induced exacerbations in asthmatic children in vivo.

Acute viral bronchiolitis in infants and young children

Anya Deborah Pat Jones Strickland Holt BSc MSc PhD PhD PhD, DSc, FRCPath, FRCPI, FAA Honorary Research Associate Head, Pregnancy and Early Life

Using Systems Biology to understand asthma exacerbations and develop better treatments

Alexander Anthony Deborah Pat Larcombe Kicic Strickland Holt BScEnv (Hons) PhD BSc (Hons) PhD PhD PhD, DSc, FRCPath, FRCPI, FAA Honorary Research

Effect of human rhinovirus infection on airway epithelium tight junction protein disassembly and transepithelial permeability

HRV-1B infection directly alters human airway epithelial TJ expression leading to increased epithelial permeability potentially via antiviral response of IL-15

Interferon regulatory factor 7 regulates airway epithelial cell responses to human rhinovirus infection

IRF7 regulates the expression of genes involved in antiviral immunity, inflammation, and the response to oxidative stress during HRV infections in HBE cells

Distinguishing benign from pathologic TH2 immunity in atopic children

In addition to its role in blocking TH2 effector activation in the late-phase allergic response, IL-10 is a known IgG1 switch factor