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Chair, John S. Strauss Professor and HeadProfessor of Dermatology
Office: 40040 Pomerantz Family Pavilion200 Hawkins DriveIowa City, IA 52242
Office Phone: 319-356-3609
BS, Zoology, Michigan State UniversityMD, Medicine, University of Michigan Medical School
Internship, Hennepin County Medical Center, Minneapolis, MNResidency, Dermatology, University of Michigan, Ann Arbor, MIFellowship, NIH Research, Cell Physiology, Dermatology, University of Michigan, Ann Arbor, MI
State of Iowa Medical License, Iowa Board of MedicineState of Michigan Medical License, Michigan Board of MedicineBoard Certified, American Board of DermatologyBoard Certified, National Board of Medical Examiners
Interdisciplinary Graduate Program in Translational Biomedicine
The overall goal of the current research in my laboratory is to better understand the pathogenesis of the organ-specific autoimmune blistering diseases, such as bullous pemphigoid. Bullous pemphigoid (BP) is an blistering skin disease skin characterized by development of autoantibodies against BP180, a cell-substrate attachment protein. Early studies of the pathogenesis of BP were focused on autoantibodies of the IgG class; however, findings from our work and others have made it clear that IgE class autoantibodies also play a critical role in this disease process. We have shown that 90% of BP patients produce IgE autoantibodies that target the same small antigenic region of BP180 (termed NC16A) that is recognized by IgG autoantibodies. Further, BP IgE, when passively transferred into a xenograft murine model, can replicate the early phase of BP lesion development. This was the first demonstration of the pathogenicity of human IgE in an autoimmune disease. Treatment of basophils isolated from BP patients with the NC16A peptide was shown to induce specific degranulation of the cells, suggesting one mechanism by which IgE may contribute to lesion development. Recently we have utilized our research on IgE for the basis of a clinical trials of anti-IgE therapy in BP. Our future goals are to further delineate the role of IgE autoantibodies and effectors cells such as eosinophils and mast cells in BP and to utilize this information to identify additional novel therapies for autoimmune diseases.
As a physician-scientist one of my major goals is to translate findings from the laboratory into improved diagnostics and or therapies for patients.
Missing the target: characterization of bullous pemphigoid patients who are negative using the BP180 enzyme-linked immunosorbant assay.
Jour Am Acad Derm.
2013 March. 68(3):395-403.
The Dermatology Foundation: partnerships and programs focused on the future.
Journal of Investigative Dermatology.
Erythema migrans: a spectrum of histopathologic changes.
AM J Dermatopath.
2012 December. 34(8):834-7.
Cryptic esophageal pemphigus vulgaris despite apparent clinical remission.
J Am Acad Dermatol.
FA role for IgE receptor expression on eosinophils in BP.
J Invest Derm.
FceRI expression by eosinophils in BP and a potential pathogenic role in eosinophil degranulation.
J Invest Dermatol.
Functional characterization of an IgE-class monoclonal antibody specific for the bullous pemphigoid autoantigen, BP180.
Monoclonal antibody BP180 against bullous pemphigoid antigen-2 type XVII collagen.
Numerous skin-colored papules on the face and neck.
TNF-α is critical for the autoimmune skin blistering disease bullous pemphigoid.
Date Last Modified: 09/18/2014 -
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