Emma Guttman-Yassky
Emma Guttman-Yassky is the System Chair of the Department of Dermatology and Waldman professor of dermatology and immunology at the Icahn School of Medicine at Mount Sinai in New York. She is also director of the, and its Inflammatory Skin Disease Laboratory.
According to Google Scholar she has an h-index of 106.
Education
Guttman received her MD from Sackler School of Medicine in 1996. While completing her dermatology residency at the Rambam Medical Center, she pursued postgraduate studies in dermatology and basic sciences at the Sackler Faculty of Medicine. She went on to study internal medicine during her translational year at Memorial Sloan-Kettering Cancer Center in 2008. Before completing her dermatology residency at Weill Cornell Medical College in 2011, she also received her PhD in 2010 for her thesis on clinical and molecular aspects of Classic Kaposi’s Sarcoma at Bar-Ilan University.Research
Dr. Guttman’s research made breakthrough discoveries on the immunologic basis of atopic dermatitis/eczema and alopecia areata as well as scarring alopecia. She is the first to identify in humans a distinct population of T-cells that independently produce IL-22 without co-producing IL-17, framing the concept that in humans, Th22 T-cells are distinct from Th17 T-cells. Guttman has also designed a clinical trial that was funded by the NIH/NIAMS, utilizing an anti-IL-22 antibody - the first to explore the biological effects of blocking IL-22 on AD. Additionally, she established the reversibility of AD and defined a series of therapeutic response-biomarkers that are now implemented in testing of novel therapeutics.Dr. Guttman’s research identified that different AD subsets differ in their immune polarization, enabling a personalized medicine approach. Her lab is currently studying the contribution of specific Th2-, Th17/IL-23-, and Th22-targeting treatments to different AD phenotypes.
More recently, her studies extended to other inflammatory skin diseases, where they have also made significant observations. They have shown that human allergic contact dermatitis is not a single entity, and various allergens induce differential immune polarizations. They have also redefined the molecular maps of AA, associating its molecular profile with Th1/IFN, Th2, and IL-23 activation. They initiated clinical trials with specific or broad agents that are now identifying which cytokine pathways are pathogenic in AA.