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Decoding Cellular And Molecular Mechanisms Of Skin Allergic Sensitization In The Atopic March

Reference : PhD Mei Li

Offer publication : Jan. 24, 2018

Atopic diseases, including asthma, allergic rhinitis (hay fever), atopic dermatitis (AD, eczema) and food allergy, are major health concerns with increasing prevalence worldwide. These diseases affect a large proportion of the population results in considerable morbidity, and are, in some circumstances, life-threatening. Asthma affects about 300 million people worldwide, and according to WHO estimates, kills approximately 250,000 people each year. Moreover, it is a leading cause of hospitalization among young children, representing a heavy burden to health care cost. Unfortunately, a long term effective treatment of asthma is still missing. Most of the current treatments, including steroid therapies and b2-adrenoceptor agonists, contribute in controlling the inflammation and relieving airway symptoms, but fail to cure the disease. It has long been known that being atopic (allergic) and having one allergic disease increases the likelihood of developing other allergic diseases during a person’s lifetime. Most strikingly, AD often precedes asthma/allergic rhinitis, referred as the “atopic march”. With no pharmacological cure for asthma in sight, there is a great need for drugs/strategies which can halt the atopic march.


Our goal of this project is to achieve a better understanding of the atopic march by decoding the cellular and molecular mechanisms of allergic sensitization occurring in AD skin, a critical step in the “atopic march”. Using mouse models that we recently established, combined with mouse genetic tools and cellular and molecular biology approaches, we aim to identify and explore how the AD skin-derived factors, including the cytokine thymic stromal lymphopoietin (TSLP) and others, critically control the T helper cell (Th2/Th17) and Follicular helper T (Tfh) cell responses during the skin allergen sensitization, which subsequently trigger the development of asthma. We also collaborate with partners to explore the relevance of our findings to human disease and achieve translational potential, by performing studies with primary cells and tissue samples from patients. Our results are expected to pave the way toward identifying biomarkers for prediction and targets for stopping the atopic march.


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Application Deadline : Nov. 1, 2018

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