This week we profile a recent publication in the Journal of Immunology from the laboratory
of Dr. Scott Tebbutt (far left) at the University of British Columbia.
Can you provide a brief overview of your lab’s current research focus?
Our research is a multidisciplinary collaboration that investigates respiratory diseases such as allergic asthma, allergic rhinitis, and allergic bronchopulmonary aspergillosis. Our approach combines laboratory-based molecular and cellular measurement of biospecimens donated from exquisitely phenotyped human subjects, with cutting-edge data analytics and bioinformatics, in order to study various aspects of the pathophysiology of these diseases. In particular, we are interested in identifying biomarkers and molecular signatures through an integration of omics-based data.
What is the significance of the findings in this publication?
We discovered systemic immune response signatures that were highly correlated to upper airway clinical symptom phenotypes of allergic rhinitis individuals who were undergoing nasal allergen challenge (i.e., allergen was directly delivered to the nasal mucosa). These systemic signatures were significantly different from healthy non-allergic individuals, and were associated with specific cell type frequencies in peripheral blood. Our approach may have utility for investigating mechanisms of action of allergic rhinitis treatments, and our molecular signatures may serve as more objective measurements of allergic rhinitis symptoms.
What are the next steps for this research?
Our systemic immune response signatures were identified in individuals who were allergic to cats, which represents a persistent (or perennial) allergic rhinitis. We are testing the reproducibility of the immune gene signatures in individuals with seasonal (or intermittent) allergic rhinitis, such as birch allergy and ragweed allergy (pollen allergy). Future studies will consider frequencies of more specific leukocyte subsets in order to elaborate the systemic immune response signature approach.
This research was funded by:
This work was supported by Adiga Life Sciences, the Allergy, Genes and the Environment Networks for Centres of Excellence (AllerGen NCE), Circassia Ltd., Mitacs Accelerate, and the Prevention of Organ Failure (PROOF) Centre of Excellence.