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Photo of Janet Fairley

Janet Fairley

Professor,  Dermatology

Contact Information

Phone: +1 319 356 3609
Email: janet-fairley@uiowa.edu
Web:

Education

BS, Zoology, Michigan State University, High Honors
MD, Medicine, University of Michigan Medical School
Internship, Hennepin County Medical Center
Residency, Dermatology, University of Michigan
Fellowship, Cell Physiology, Dermatology, University of Michigan

Appointments

Primary: Dermatology

Centers and Program Affiliations


Research Interests

blistering diseases of the skin, epidermal cell physiology, dermatology education

MeSH Terms from Publications

Pemphigoid, Bullous, Non-Fibrillar Collagens, Autoantibodies, Pemphigus, Autoantigens, Desmoglein 3, Humans, Desmoglein 1, Immunoglobulin G, Skin, Cadherins, Immunoglobulin E, Epitopes, Animals, Mice, Inbred BALB C, Mice, Skin Diseases, Female, Collagen Type VII, Epidermis, Calmodulin, Immunoblotting, Blister, Desmogleins, Fluorescent Antibody Technique, Direct

Research Summary

The overall goal of the Fairley laboratory is to better understand the pathogenesis of the autoimmune blistering diseases of the skin. These disorders are primarily autoantibody-mediated and through a better understanding of how these antibodies develop and lead to blistering, we hope to develop new therapeutic interventions. Bullous pemphigoid (BP) is a blistering disease of the skin characterized by autoantibodies directed against BP180, also termed collagen XVII, a cell-substrate attachment protein of the hemisdesmosome. Antibodies of the IgG1 and IgG4 subclass historically have been the focus of most studies of the pathogenesis of this disorder. Work in the Fairley laboratory has shown that during the initial urticarial phase of the disease 70% of BP patients have elevated total IgE levels. IgE autoantibodies that specifically target BP180 have been identified in 90% of these patients. These IgE autoantibodies predominantly target the same region of the BP antigen as the IgG class autoantibodies (NC16A). Basophils from untreated BP patients will degranulate when exposed to the NC16A region of BP180. Utilizing human skin grafted to nu/nu mice the Fairley laboratory has demonstrated that purified IgE from BP patients results in formation of urticarial plaques with histologic separation of the skin through the basement membrane zone. Electron microscopy of these lesions indicates degranulation of mast cells and infiltration of lymphocytes, PMNs and eosinophils. On going studies aim to differentiate the IgE effects on mast cells and keratinocytes using real-time PCR, cytokine antibody arrays and ELISA. In addition, the development of IgE class autoantibodies is other blistering disorders is being studied. A pilot project examining the effect of the humanized anti-IgE monoclonal antibody, omalizumab, in BP patients has been developed. Pemphigus vulgaris (PV) is characterized by development of autoantibodies that target the desmosomal protein desmoglein 3. These autoantibodies lead to loss of cell-cell attachment between keratinocytes that results in epidermal separation and blister formation. TNF has been hypothesized to play a role in B cell maturation and on-going production of autoantibodies. The Fairley laboratory is part of a multicenter trial of infliximab in the treatment of PV patients. This study will also include an assessment of B cells maturation and autoantibody production

Recent Publications


Show publications
  1. Erythema migrans: a spectrum of histopathologic changes. Am J Dermatopathol 34(8):834-7, 2012. [PubMed]
  2. Cryptic esophageal pemphigus vulgaris despite apparent clinical remission. J Am Acad Dermatol 67(5):e213-4, 2012. [PubMed]
  3. Successful treatment of bullous pemphigoid with omalizumab. Arch Dermatol 148(11):1241-3, 2012. [PubMed]
  4. Numerous skin-colored papules on the face and neck. Arch Dermatol 148(7):849-54, 2012. [PubMed]
  5. Role of IgE in bullous pemphigoid: a review and rationale for IgE directed therapies. G Ital Dermatol Venereol 147(3):251-7, 2012. [PubMed]
  6. Functional characterization of an IgE-class monoclonal antibody specific for the bullous pemphigoid autoantigen, BP180. Hybridoma (Larchmt) 31(2):111-7, 2012. [PubMed]
  7. Monoclonal antibody BP180 against bullous pemphigoid antigen-2 type XVII collagen. Hybridoma (Larchmt) 31(2):146-7, 2012. [PubMed]
  8. Definitions and outcome measures for bullous pemphigoid: recommendations by an international panel of experts. J Am Acad Dermatol 66(3):479-85, 2012. [PubMed]
  9. Cutaneous Rosai-Dorfman disease following pneumococcal vaccination. J Am Acad Dermatol 65(4):890-2, 2011. [PubMed]
  10. FcR-independent effects of IgE and IgG autoantibodies in bullous pemphigoid. J Immunol 187(1):553-60, 2011. [PubMed]