Lisa A. Beck, MD, has dedicated a quarter century to the quest for a safe, effective treatment for eczema and chronic urticaria, and her research was key to the development of dupilumab (Dupixent), the first biologic drug FDA approved for adults with moderate to severe eczema.
1
Dr Beck has also helped uncover mechanisms responsible for skin inflammation in eczema that may explain its relationship to skin infections and environmental allergies. The Dean’s Professor of Dermatology and Medicine at the University of Rochester Medical Center holds leadership positions with numerous organizations including the National Eczema Association, International Eczema Council, Society for Investigative Dermatology, and is principal investigator of the National Institutes of Health/National Institute for Allergy and Infectious Diseases-funded Atopic Dermatitis Research Network, which has amassed the largest atopic dermatitis (AD) registry in the world.
In this interview with The Dermatologist, Dr Beck describes her contributions to science and her opinion about why dermatologists tend to be happy.
Q. What is your role as the Dean’s Professor of Dermatology and Medicine at the University of Rochester Medical Center?
a. I’ve been at the University of Rochester Medical Center for almost 11 years and was recently given an endowed position funded by the Dean’s office as acknowledgement of my contribution to the Departments of Dermatology and Pathology and the Division of allergy, immunology, and rheumatology. I am the founding director of the Dermatology Clinical Trials Unit at the University of Rochester.
Q. How have you combined dermatology, immunology, allergology, and pathology as your areas of expertise?
a. My board certification is in dermatology only, but I spent almost 16 years at the Johns Hopkins Asthma and Allergy Center where my research laboratory was housed and worked in a multidisciplinary group of scientists and physician-scientists focused on the study of all allergic conditions. My wet bench research focused on understanding and characterizing allergic inflammation—primarily in the skin—although I also did studies relevant for diseases in the nose or lower airway. This experience solidified my relationship with allergists and immunologists. Many of my observations relied on tissue histopathology and this became a strength of my research program and this logically aligned me with pathology.
Q. How did you decide on a career in dermatology?
a. My immediate intent upon graduation from medical school was to become a primary care focused internist, but 2 years into my internal medicine training, I began to question whether this was the best choice for me. I realized I was a visual learner and saw patterns not only in the study of art history as an undergraduate but also as a physician at the bedside. The ability to quickly assess patterns on the skin surface is a huge advantage for a dermatologist and once I realized this I knew I had found my niche.
Article continues on page 2
Q. What influenced your focus on AD and urticaria?
a. Dermatologists are such a happy group because we make almost all of our patients a little better and many of them we make a lot better. Early in my career I realized that although I wasn’t saving people’s lives in the same way I think an internist does, nevertheless I got quite a bit of satisfaction from the practice of dermatology as patients from all walks of life are remarkably compliant with skin treatments probably because they get to see the disease improve and are often bothered by the disease cosmetically. A few years into my career I turned my attention to more significant medical dermatology diseases in part to feel that I was making a more significant impact in patients’ health and because of my strong background in internal medicine. As soon as I moved to the Johns Hopkins Asthma and Allergy Center—where I was surrounded by allergists—it just made logical sense that I would focus my research and clinical efforts on AD and chronic urticaria.
Q. What have been some of your areas of research?
a. My research interests are in 3 interrelated areas. First, my lab has focused on characterizing the epithelial tight junction (TJ) defects at the molecular level in AD—the most common inflammatory skin disease in man. Numerous projects radiate from that central theme and include: (1) how do these defects differ in other inflammatory skin diseases such as chronic urticaria, psoriasis, cutaneous T-cell lymphoma; (2) what effects do various pharmacologic agents have on TJ function and structure; and (3) can protease containing allergens or microbes affect TJ function, and if so, how.
A second area of focus is evaluating the magnitude and character of the microbial responsiveness of keratinocytes (cutaneous epithelial cells) from AD patients compared with nonatopic healthy controls. When differences are noted we are trying to determine the basis for these differences and believe this line of inquiry may explain AD patients’ susceptibility to colonization and infection with numerous bacteria, viruses, and even yeast.
Our third area has been to understand why there is such a paucity of tissue neutrophils in lesions from patients with AD. These studies are not as advanced, but suggest that there are phenotypic differences in AD neutrophils’ responsiveness to the potent chemoattractant, IL-8 (CXCL8) compared with nonatopic controls.
Q. What have some of your contributions to science in general and dermatology specifically been?
a. My lab was the first to demonstrate that leukocytes’ activation status affected their in vivo responsiveness to intradermally injected chemokines, and that chemokines also act on structural cells, implicating chemokines as mediators of fibrosis and/or epithelial barrier repair. More recently, my lab has been exploring the dynamic interaction between the skin barrier and the innate and adaptive immune systems. I was the first to describe and characterize epidermal TJ defects in AD and ongoing studies are evaluating whether these defects develop as a consequence of tissue inflammation or microbial flora, which is highly altered in AD patients.
Q. What drives you?
a. We have recently entered a golden era for AD with many exciting new advances in our understanding of disease pathogenesis and many new and more targeted therapies. This is long overdue as it has been almost 15 years since tacrolimus and pimecrolimus were FDA approved. We are so excited that this shocking dearth of safe and effective AD therapies will soon change.
References
1. Beck LA, Thaçi D, Hamilton JD, et al. Dupilumab treatment in adults with moderate-to-severe atopic dermatitis. N Eng J Med. 2014;371(2):130-139.
Lisa A. Beck, MD, has dedicated a quarter century to the quest for a safe, effective treatment for eczema and chronic urticaria, and her research was key to the development of dupilumab (Dupixent), the first biologic drug FDA approved for adults with moderate to severe eczema.
1
Dr Beck has also helped uncover mechanisms responsible for skin inflammation in eczema that may explain its relationship to skin infections and environmental allergies. The Dean’s Professor of Dermatology and Medicine at the University of Rochester Medical Center holds leadership positions with numerous organizations including the National Eczema Association, International Eczema Council, Society for Investigative Dermatology, and is principal investigator of the National Institutes of Health/National Institute for Allergy and Infectious Diseases-funded Atopic Dermatitis Research Network, which has amassed the largest atopic dermatitis (AD) registry in the world.
In this interview with The Dermatologist, Dr Beck describes her contributions to science and her opinion about why dermatologists tend to be happy.
Q. What is your role as the Dean’s Professor of Dermatology and Medicine at the University of Rochester Medical Center?
a. I’ve been at the University of Rochester Medical Center for almost 11 years and was recently given an endowed position funded by the Dean’s office as acknowledgement of my contribution to the Departments of Dermatology and Pathology and the Division of allergy, immunology, and rheumatology. I am the founding director of the Dermatology Clinical Trials Unit at the University of Rochester.
Q. How have you combined dermatology, immunology, allergology, and pathology as your areas of expertise?
a. My board certification is in dermatology only, but I spent almost 16 years at the Johns Hopkins Asthma and Allergy Center where my research laboratory was housed and worked in a multidisciplinary group of scientists and physician-scientists focused on the study of all allergic conditions. My wet bench research focused on understanding and characterizing allergic inflammation—primarily in the skin—although I also did studies relevant for diseases in the nose or lower airway. This experience solidified my relationship with allergists and immunologists. Many of my observations relied on tissue histopathology and this became a strength of my research program and this logically aligned me with pathology.
Q. How did you decide on a career in dermatology?
a. My immediate intent upon graduation from medical school was to become a primary care focused internist, but 2 years into my internal medicine training, I began to question whether this was the best choice for me. I realized I was a visual learner and saw patterns not only in the study of art history as an undergraduate but also as a physician at the bedside. The ability to quickly assess patterns on the skin surface is a huge advantage for a dermatologist and once I realized this I knew I had found my niche.
Article continues on page 2
Q. What influenced your focus on AD and urticaria?
a. Dermatologists are such a happy group because we make almost all of our patients a little better and many of them we make a lot better. Early in my career I realized that although I wasn’t saving people’s lives in the same way I think an internist does, nevertheless I got quite a bit of satisfaction from the practice of dermatology as patients from all walks of life are remarkably compliant with skin treatments probably because they get to see the disease improve and are often bothered by the disease cosmetically. A few years into my career I turned my attention to more significant medical dermatology diseases in part to feel that I was making a more significant impact in patients’ health and because of my strong background in internal medicine. As soon as I moved to the Johns Hopkins Asthma and Allergy Center—where I was surrounded by allergists—it just made logical sense that I would focus my research and clinical efforts on AD and chronic urticaria.
Q. What have been some of your areas of research?
a. My research interests are in 3 interrelated areas. First, my lab has focused on characterizing the epithelial tight junction (TJ) defects at the molecular level in AD—the most common inflammatory skin disease in man. Numerous projects radiate from that central theme and include: (1) how do these defects differ in other inflammatory skin diseases such as chronic urticaria, psoriasis, cutaneous T-cell lymphoma; (2) what effects do various pharmacologic agents have on TJ function and structure; and (3) can protease containing allergens or microbes affect TJ function, and if so, how.
A second area of focus is evaluating the magnitude and character of the microbial responsiveness of keratinocytes (cutaneous epithelial cells) from AD patients compared with nonatopic healthy controls. When differences are noted we are trying to determine the basis for these differences and believe this line of inquiry may explain AD patients’ susceptibility to colonization and infection with numerous bacteria, viruses, and even yeast.
Our third area has been to understand why there is such a paucity of tissue neutrophils in lesions from patients with AD. These studies are not as advanced, but suggest that there are phenotypic differences in AD neutrophils’ responsiveness to the potent chemoattractant, IL-8 (CXCL8) compared with nonatopic controls.
Q. What have some of your contributions to science in general and dermatology specifically been?
a. My lab was the first to demonstrate that leukocytes’ activation status affected their in vivo responsiveness to intradermally injected chemokines, and that chemokines also act on structural cells, implicating chemokines as mediators of fibrosis and/or epithelial barrier repair. More recently, my lab has been exploring the dynamic interaction between the skin barrier and the innate and adaptive immune systems. I was the first to describe and characterize epidermal TJ defects in AD and ongoing studies are evaluating whether these defects develop as a consequence of tissue inflammation or microbial flora, which is highly altered in AD patients.
Q. What drives you?
a. We have recently entered a golden era for AD with many exciting new advances in our understanding of disease pathogenesis and many new and more targeted therapies. This is long overdue as it has been almost 15 years since tacrolimus and pimecrolimus were FDA approved. We are so excited that this shocking dearth of safe and effective AD therapies will soon change.
References
1. Beck LA, Thaçi D, Hamilton JD, et al. Dupilumab treatment in adults with moderate-to-severe atopic dermatitis. N Eng J Med. 2014;371(2):130-139.
Lisa A. Beck, MD, has dedicated a quarter century to the quest for a safe, effective treatment for eczema and chronic urticaria, and her research was key to the development of dupilumab (Dupixent), the first biologic drug FDA approved for adults with moderate to severe eczema.
1
Dr Beck has also helped uncover mechanisms responsible for skin inflammation in eczema that may explain its relationship to skin infections and environmental allergies. The Dean’s Professor of Dermatology and Medicine at the University of Rochester Medical Center holds leadership positions with numerous organizations including the National Eczema Association, International Eczema Council, Society for Investigative Dermatology, and is principal investigator of the National Institutes of Health/National Institute for Allergy and Infectious Diseases-funded Atopic Dermatitis Research Network, which has amassed the largest atopic dermatitis (AD) registry in the world.
In this interview with The Dermatologist, Dr Beck describes her contributions to science and her opinion about why dermatologists tend to be happy.
Q. What is your role as the Dean’s Professor of Dermatology and Medicine at the University of Rochester Medical Center?
a. I’ve been at the University of Rochester Medical Center for almost 11 years and was recently given an endowed position funded by the Dean’s office as acknowledgement of my contribution to the Departments of Dermatology and Pathology and the Division of allergy, immunology, and rheumatology. I am the founding director of the Dermatology Clinical Trials Unit at the University of Rochester.
Q. How have you combined dermatology, immunology, allergology, and pathology as your areas of expertise?
a. My board certification is in dermatology only, but I spent almost 16 years at the Johns Hopkins Asthma and Allergy Center where my research laboratory was housed and worked in a multidisciplinary group of scientists and physician-scientists focused on the study of all allergic conditions. My wet bench research focused on understanding and characterizing allergic inflammation—primarily in the skin—although I also did studies relevant for diseases in the nose or lower airway. This experience solidified my relationship with allergists and immunologists. Many of my observations relied on tissue histopathology and this became a strength of my research program and this logically aligned me with pathology.
Q. How did you decide on a career in dermatology?
a. My immediate intent upon graduation from medical school was to become a primary care focused internist, but 2 years into my internal medicine training, I began to question whether this was the best choice for me. I realized I was a visual learner and saw patterns not only in the study of art history as an undergraduate but also as a physician at the bedside. The ability to quickly assess patterns on the skin surface is a huge advantage for a dermatologist and once I realized this I knew I had found my niche.
Article continues on page 2
Q. What influenced your focus on AD and urticaria?
a. Dermatologists are such a happy group because we make almost all of our patients a little better and many of them we make a lot better. Early in my career I realized that although I wasn’t saving people’s lives in the same way I think an internist does, nevertheless I got quite a bit of satisfaction from the practice of dermatology as patients from all walks of life are remarkably compliant with skin treatments probably because they get to see the disease improve and are often bothered by the disease cosmetically. A few years into my career I turned my attention to more significant medical dermatology diseases in part to feel that I was making a more significant impact in patients’ health and because of my strong background in internal medicine. As soon as I moved to the Johns Hopkins Asthma and Allergy Center—where I was surrounded by allergists—it just made logical sense that I would focus my research and clinical efforts on AD and chronic urticaria.
Q. What have been some of your areas of research?
a. My research interests are in 3 interrelated areas. First, my lab has focused on characterizing the epithelial tight junction (TJ) defects at the molecular level in AD—the most common inflammatory skin disease in man. Numerous projects radiate from that central theme and include: (1) how do these defects differ in other inflammatory skin diseases such as chronic urticaria, psoriasis, cutaneous T-cell lymphoma; (2) what effects do various pharmacologic agents have on TJ function and structure; and (3) can protease containing allergens or microbes affect TJ function, and if so, how.
A second area of focus is evaluating the magnitude and character of the microbial responsiveness of keratinocytes (cutaneous epithelial cells) from AD patients compared with nonatopic healthy controls. When differences are noted we are trying to determine the basis for these differences and believe this line of inquiry may explain AD patients’ susceptibility to colonization and infection with numerous bacteria, viruses, and even yeast.
Our third area has been to understand why there is such a paucity of tissue neutrophils in lesions from patients with AD. These studies are not as advanced, but suggest that there are phenotypic differences in AD neutrophils’ responsiveness to the potent chemoattractant, IL-8 (CXCL8) compared with nonatopic controls.
Q. What have some of your contributions to science in general and dermatology specifically been?
a. My lab was the first to demonstrate that leukocytes’ activation status affected their in vivo responsiveness to intradermally injected chemokines, and that chemokines also act on structural cells, implicating chemokines as mediators of fibrosis and/or epithelial barrier repair. More recently, my lab has been exploring the dynamic interaction between the skin barrier and the innate and adaptive immune systems. I was the first to describe and characterize epidermal TJ defects in AD and ongoing studies are evaluating whether these defects develop as a consequence of tissue inflammation or microbial flora, which is highly altered in AD patients.
Q. What drives you?
a. We have recently entered a golden era for AD with many exciting new advances in our understanding of disease pathogenesis and many new and more targeted therapies. This is long overdue as it has been almost 15 years since tacrolimus and pimecrolimus were FDA approved. We are so excited that this shocking dearth of safe and effective AD therapies will soon change.
References
1. Beck LA, Thaçi D, Hamilton JD, et al. Dupilumab treatment in adults with moderate-to-severe atopic dermatitis. N Eng J Med. 2014;371(2):130-139.
