Allergic airway inflammations, such as asthma, are an increasingly important disease caused by bronchial inflammation and characterized by bronchial hyper-responsiveness and intermittent airway obstruction with an underlying Th2 cell-biased inflammatory response in the airways. The disease is currently treated with bronchodilators or anti- inflammatory drugs such as corticosteroids, leukotriene modifiers, and anti-IgE therapy, etc. However, the current treatments are not curative and some patients do not respond well to intense anti-inflammatory therapies. Additionally, the use of long-term steroids may result in many undesired side effects. For this reason, novel and more effective intervening strategies are greatly needed and explored. Targeting of the functions of Th2 cells and their products have been proposed as an effective strategy for the development of potential stand-alone treatments for allergic asthma. The reduction or elimination of allergen-specific Th2 cells in early disease development is expected to reduce the consequences of repeated allergic inflammatory. Hence, efficient delivery of immunotherapeutic proteins into the airway tract could effectively and directly interfere with allergen-specific Th2 cell activation in its earliest phaseof function. However, the polarized epithelial monolayer lining the airway forms mucosal barrier which is impervious to macromolecule diffusion. This barrier poses a major difficulty for an efficient delivery of immunotherapeutic proteins to access and cross-talk with underlying immune effector cells, such as Th2 cells, in the airway. Our recent studies have shown that human CD23 receptor is functionally capable of transporting IgE antibody across human lung and bronchial epithelial cells. In this study, we further propose to examine the feasibility of CD2 to deliver the immunotherapeutic proteins, which are targeted to interfere with CD4 Th2 cell function, across airway mucosal barrier in a mouse allergy model. These studies, therefore, are very likely to lead to greatly improved novel therapies that protect against and potentially cure asthma and allergic diseases.

Public Health Relevance

CD23-mediated immunotherapy on airway inflammation Airway inflammation, asthma, is among the most common diseases in both infant and adult. CD23 is capable of transporting IgE across airway epithelial cells. This study will explore the feasibility whether CD23 can deliver an immunotherapeutic protein to modulate or dampen the development of airway allergic inflammation.

National Institute of Health (NIH)
National Institute of Allergy and Infectious Diseases (NIAID)
Exploratory/Developmental Grants (R21)
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Hypersensitivity, Autoimmune, and Immune-mediated Diseases Study Section (HAI)
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Dong, Gang
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University of Maryland College Park
Veterinary Sciences
Schools of Earth Sciences/Natur
College Park
United States
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Palaniyandi, S; Liu, X; Periasamy, S et al. (2015) Inhibition of CD23-mediated IgE transcytosis suppresses the initiation and development of allergic airway inflammation. Mucosal Immunol 8:1262-74
Palaniyandi, Senthilkumar; Mitra, Arindam; Herren, Christopher D et al. (2013) LuxS contributes to virulence in avian pathogenic Escherichia coli O78:K80:H9. Vet Microbiol 166:567-75