Chronic Idiopathic Urticaria: Mapping a Brighter Future

Dr. Allen Kaplan graduated from Downstate Medical School (SUNY-Brooklyn) and completed his Residency in Medicine at Strong Memorial Hospital in Rochester, NY. From there he spent two years as a Clinical Fellow in the Arthritis and Rheumatism Branch of The National Institute of Arthritis and Metabolic Diseases followed by a Fellowship in Allergy and Clinical Immunology at the Harvard Medical School - Robert B. Brigham Hospital. He then returned to NIH as Head of the Allergic Diseases Section of NIAID where he remained for six years (1972-1978) and established the Allergic Diseases Center at NIH. Dr. Kaplan next moved to Stony Brook University where he was Head of the Division of Allergy, Rheumatology, and Clinical Immunology for 9 years, and was then named Chairman of the Department of Medicine. He remained at Stony Brook for 19 years and then came to The Medical University of South Carolina as Professor of Medicine. He is board certified in Internal Medicine, Allergy and Clinical Immunology, Rheumatology and Diagnostic Laboratory Immunology.
 
Dr. Kaplan was President of AAAAI in 1989, President of the Clinical Immunology Society in 1990, and President of The World Allergy Organization  (WAO/IAACI) from 2000-2003. Author of over 325 publications, his major areas of interest are the mechanisms for production of bradykinin and its role in human disease, as well as the pathogenesis and treatment of urticaria and angioedema. He edited The Journal of The World Allergy Organization for five years, edited the textbook "Allergy", is Co-Editor, with Dr. Malcolm Greaves, of a text entitled, Urticaria and Angioedema", and is Co-Editor of the two-volume textbook "Allergy and Allergic Diseases".

Dr. Beck's laboratory focuses on understanding the interaction between skin barrier defects and the innate and adaptive immune system in subjects with atopic dermatitis, the most common inflammatory skin disorder. Her laboratory was the first to describe epidermal tight junction (TJ) defects in this disease. They continue to characterize these TJ defects at the molecular level and hope to determine whether these defects develop on a genetic, epigenetic or acquired basis. A number of therapeutic agents are being tested in vitro and in vivo for their ability to repair TJ defects. Her laboratory has also identified that several innate immune pathways including NOD2, TLR2 and 3 enhance epidermal TJ function. Her laboratory is also interested in understanding why subjects with atopic dermatitis are chronically colonized with bacteria, and more frequently infected with both bacteria and viruses. The working hypothesis is that AD subjects have an inadequate epidermal innate immune response to these cutaneous pathogens. Dr. Beck's clinical and laboratory work on atopic dermatitis has been supported by grants from the National Eczema Association, NIH/NIAID, NIH/NIAMS, Dermatology Foundation, and from biotechnology and pharmaceutical industries. She is a subcontractor on the NIH/NIAID funded Atopic Dermatitis Research Network (ADRN), which has amassed the largest registry of well-characterized subjects with Atopic Dermatitis in the US.