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Asthma • cytokines (IL-4/IL-13/IL-17) • recombinant retroviruses • cell penetrating peptides • animal models
My research focuses on two main areas. For the first project, we are investigating mechanisms by which different T lymphocyte subsets orchestrate airway inflammatory responses in allergic airways diseases such as asthma. Th2 type lymphocytes are well-characterized mediators in both humans and in animal models of asthma. More recently, new subsets of T lymphocytes which produce an inflammatory mediator called IL-17 have been implicated in allergic airways disease. We are using well-established murine models of allergic airways disease, recombinant cytokines, as well as recombinant retrovirus technologies to characterize how IL-17 expressing cells modulate Th2 type inflammation in the lung. For the second project in my lab we are investigating novel mechanisms by which a protein called STAT6 initiates allergic responses in the airways. For these studies we are using a special peptide that was designed to enter cells and bind to and inhibit STAT6. We are assessing the ability of this peptide to inhibit the initiation of the allergic response.
Wang, Y., Li, Y., J. Shan, E.D. Fixman, and C.M. McCusker. (2011) Effective treatment of experimental ragweed-induced asthma with STAT-6-IP, a topically delivered cell penetrating peptide. Clin. Exp. Allergy. 41:1622-1630.
Kinyanjui, M.W., J. Shan, E.M. Nakada, S.T. Qureshi, and E.D. Fixman. (2013) Dose-dependent effects of IL-17 on IL-13-induced airway inflammatory responses and airway hyperresponsiveness. J. Immunol. 190:3859-3868.