Welcome to the Beck Lab

The Beck lab has had a longstanding interest in characterizing cutaneous allergic inflammation with a specific focus on Atopic Dermatitis (or eczema). The lab was the first to demonstrate that leukocytes’ activation status affected their in vivo responsiveness to intradermally injected chemokines.  Additionally, Dr. Beck demonstrated that chemokines also act on structural cells, implicating chemokines as mediators of fibrosis and/or epithelial barrier repair. More recently, her laboratory has been exploring the dynamic interaction between the skin barrier and the innate and adaptive immune systems.  She was the first to describe and characterize epidermal tight junction (TJ) defects in atopic dermatitis. Ongoing studies are evaluating whether these defects develop as a consequence of tissue inflammation or microbial flora, which is highly altered in AD subjects.  The lab has observed that several innate immune pathways including NOD2, TLR2 and 3 and adaptive immune pathways such as IL-17a enhance, whereas histamine inhibits epidermal TJ function.

Another focus of the laboratory is trying to understand the role that epithelium (keratinocytes) play in epicutaneous allergen sensitization and vaccination. Dr. Beck’s clinical and laboratory work has been supported by grants from the National Eczema Association, NIH, Dermatology Foundation, and from biotech/pharmaceutical companies. She has been co-PI of the NIH/NIAID-funded Atopic Dermatitis Research Network (ADRN) since 2004, which has amassed the largest registry of deeply phenotyped Atopic Dermatitis subjects in the world. In the past 20 years, she have trained 6 undergraduates, 4 medical students, 10 post-doctoral fellows, 2 PhD candidates, and served as a thesis committee advisor for over 6 PhD or MD/PhD students.

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