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A pathogenic role for the integrin CD103 in experimental allergic airways diseaseRole for CD103 in the pathogenesis of experimental allergic airways disease in BALB/c mice through local control of CD4+ T cell and DC subset recruitment
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Attenuation of maternal inflammatory responses during pregnancy to promote normal immune and behavioral outcomes in the offspringThis study will identify how the immune system contributes to neurodevelopmental outcomes and will investigate the use of an agent from traditional medicines.
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Long-term derangement of antigen presenting cell populations in the respiratory tract following Influenza A infectionThis project investigates how different populations of cells within the respiratory tract immune system are altered during a viral infection.
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UV exposure and protection against allergic airways diseaseAsthma is a chronic inflammatory disease of the small and large conducting airway mucosa characterised by Th2 cell immunity.
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Identification and Isolation of Rodent Respiratory Tract Dendritic CellsThis chapter describes the preparation of respiratory tract tissue from both mice and rats for the isolation of respiratory tract dendritic cells (RTDC).
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Early biomarkers predictive of autismThis study aims to investigate the cellular and molecular profiles of the immune system in infants at high/low risk for Autism, as determined through clinical assessment.
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Finding the cellular explanation for recurrent asthma exacerbationsThis study is designed to identify the specific unique immune cell response that occurs in these children with recurrent disease.
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Transplacental immune modulation with a bacterial-derived agent protects against allergic airway inflammationThese data provide proof of concept supporting the rationale for developing transplacental immune reprogramming approaches for primary disease prevention
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Plasma C4d as marker for lupus nephritis in systemic lupus erythematosusIn the present study, we sought to evaluate the complement activation product C4d as a marker for lupus nephritis in systemic lupus erythematosus (SLE).
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Tumor necrosis factor α induces α1B-adrenergic receptor expression in keratinocytesOur results suggest that inflammatory cytokines released during injury stimulate α1-AR expression in keratinocytes