Annika Scheynius, Professor in Clinical Allergy Research
Johan S Alm, M.D., Ph.D. student, tel 517 76699, fax 33 57 24, email josal@mb.ks.se
Research projects: Allergies and other hypersensitivity reactions currently affect approximately 30% of the population. The aims of the project are 1) to increase understanding of the mechanisms which determine whether an exposed individual will become sensitized or not, 2) to characterize allergens and their interaction with various antigen-presenting cells, 3) to improve methods for diagnosis of allergic and inflammatory diseases, and 4) to provide knowledge on how the body´s own regulatory mechanisms can be used in prevention or therapy. Today we have facilities for immunohisto/cytochemistry, advanced microscopy and image analysis, flow cytometry, different methods for serological analysis, cell culture methods for production of monoclonoal antibodies, T cell clones, EBV transformed B cell lines, measurements of T cell proliferation and cytokine production, methods for characterization of allergens, molecular biology techniques like reverse transcriptase PCR for detection of cytokine mRNA in small tissue samples, cDNA cloning, expression systems for recombinant allergens and facilities for animal experiments.
Research results: We have shown that the confocal microscope is a usefool tool for quantitative and 3-dimensional analysis of Langerhans´cells in the skin and for localization of allergens in mites and yeast cells. In studies on the pathogenic mechanisms for atopic eczema we have found that the yeast, Pityrosporum orbiculare, which is normally present on the skin, can act as an allergen. We have cloned one of the major allergens, Mal f 1, which is a novel protein not present in other yeasts. With confocal microscopy and flow cytometry analysis we have localized this 38 kDa protein to the cell wall and found it exposed on the cell surface. Patients with atopic eczema have a T cell reactivity against P. orbiculare not seen in healthy controls. The majority of P. orbiculare reactive T cell clones established from lesional atopic skin have a Th2-like cytokine profile. We have shown that CD30 can not be used as a marker to identify Th2 cells, which has been claimed by others. Furthermore, we have found that unresponsiveness to an allergen can be induced if cell interactions between the adhesion molecules LFA-1 and ICAM-1 are blocked by monoclonal antibodies during sensitization.
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