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Allergic diseases affect an increasing number of individuals world-wide. They are caused by immune responses to proteins, often from environmental sources, that we would usually tolerate. Sensitization to allergens causes an immune response that is skewed towards a Th2-type T cell response and is often accompanied by production of allergen-specific antibodies, in particular IgE. Within the cascade of allergic reactions, the mast cell is a central player in orchestrating the immune responses and physiology. They are potently triggered by IgE to release a vast array of inflammatory mediators. We are researching several critical mast cell-derived mediators for how they influence allergy. Our work uses a diverse array of approaches: from animal models to molecular immunology.
Currently, we have projects that are focused on understanding the roles of histamine and the 4 histamine receptors on the sensitization to allergens, the recruitment of inflammatory cells into tissues and the loss of the normal tolerance mechanisms. We are also strongly interested in food allergy and have developed a number of novel approaches to model this disease. We are researching the mechanisms for loss of tolerance to peanut and egg proteins to better understand why food allergy occurs, as well as testing therapeutic approaches to treat food allergy.
Selected Publications:
Bryce PJ & Oettgen HC. Antigen Independent Effects of IgE. Curr Allergy Asthma Rep. 2005 May;5(3):186-190.
Bryce PJ, Miller ML, Miyajima I, Tsai M, Galli SJ, Oettgen HC. Immune sensitization in the skin is enhanced by antigen-independent effects of IgE. Immunity. 2004 Apr;20(4):381-92.
Gurish MF, Bryce PJ, Tao H, Kisselgof AB, Thornton EM, Miller HR, Friend DS, Oettgen HC. IgE enhances parasite clearance and regulates mast cell responses in mice infected with Trichinella spiralis. J Immunol. 2004 ;172:1139-45.
Castigli E, Scott S, Dedeoglu F, Bryce P, Jabara H, Bhan AK, Mizoguchi E, Geha RS. Impaired IgA class switching in APRIL-deficient mice. P.N.A.S. 2004 ;101:3903-8.
Alonzi T, Newton IP, Bryce PJ, Di Carlo E, Lattanzio G, Tripodi M, Musiani P, Poli V. Induced somatic inactivation of STAT3 in mice triggers the development of a fulminant form of enterocolitis. Cytokine. 2004 ;26:45-56.
Kawamoto S, Yalcindag A, Laouini D, Brodeur S, Bryce P, Lu B, Humbles AA, Oettgen H, Gerard C, Geha RS. The anaphylatoxin C3a downregulates the Th2 response to epicutaneously introduced antigen. J Clin Invest. 2004 Aug;114(3):399-407.
