报告题目： Is the nervous system more important that the immune system in itch and atopic dermatitis?
报告人： Ethan Arthur Lerner, M.D., PH.D. Associate Professor of Dermatology Massachusetts General Hospital, Harvard Medical School
报告时间：2016年5月20日（周五）16：00
报告地点： 18新利体育 神经18新利备用网站 所会议室
报告人简介：Dr. Ethan A. Lerner received his M.D. and PhD from Yale University. He is the Founder and serves as the Chairman of Lerner Medical Devices, Inc. Dr. Lerner is an Associate Professor of Dermatology at Harvard Medical School and the Massachusetts General Hospital. He is an inventor of the fiberoptic hairbrush. Dr. Lerner is interested in how things on the outside of the skin mediate effects on the inside. He co-founded Bunsen Rush Laboratories, Inc. Dr. Lerner served as a Member of Scientific Advisory Board of PPD Dermatology, Inc. He is the author of over 75 articles and holds one dozen patents.
Born into an accomplished dermatology family, Ethan Lerner, M.D., has had to ask himself if he had any choice but to join the specialty. His father, the late Aaron B. Lerner, M.D., former professor and chairman of the Yale University dermatology department, discovered melatonin and developed transplantation therapy for vitiligo. He also isolated melanocyte stimulating hormone, or MSH. Ethan's mother, Marguerite Lerner, M.D., was a dermatologist and Yale professor and an author of numerous children's books.
Selected Publications:
1. Pereira PJ, Machado GD, Danesi GM, Canevese FF, Reddy VB, Pereira TC, Bogo MR, Cheng YC, Laedermann C, Talbot S, Lerner EA, Campos MM. GRPR/PI3K?: Partners in Central Transmission of Itch. J Neurosci. 2015 Dec 9; 35(49):16272-81. PMID: 26658875.
2. Reddy VB, Sun S, Azimi E, Elmariah SB, Dong X, Lerner EA. Redefining the concept of protease-activated receptors: cathepsin S evokes itch via activation of Mrgprs. Nat Commun. 2015; 6:7864. PMID: 26216096; PMCID: PMC4520244 [Available on 01/28/16].
3. Reddy VB, Lerner EA. Plant cysteine proteases that evoke itch activate protease-activated receptors. Br J Dermatol. 2010 Sep; 163(3):532-5. PMID: 20491769; PMCID: PMC3696472.
4. Reddy VB, Iuga AO, Shimada SG, LaMotte RH, Lerner EA. Cowhage-evoked itch is mediated by a novel cysteine protease: a ligand of protease-activated receptors. J Neurosci. 2008 Apr 23; 28(17):4331-5. PMID: 18434511; PMCID: PMC2659338.
5. Lerner EA, Lerner MR, Janeway CA, Steitz JA. Monoclonal antibodies to nucleic acid-containing cellular constituents: probes for molecular biology and autoimmune disease. Proc Natl Acad Sci U S A. 1981 May; 78(5):2737-41. PMID: 6789322; PMCID: PMC319432.
报告摘要: Itch, or pruritus, can make people miserable. It is the most common symptom in dermatology yet there are few specific treatments. We aim to develop new clinical approaches and decipher the basic mechanisms that underlie this sensation and determine the molecules, receptors and channels involved in this sensation. In addition, we use advanced in vivo imaging techniques to examine the neuroanatomy of sensory fibers. As an example, the student may have the opportunity to use genetic, biochemical or imgaing techniques. For example, depending upon the timing of the project, it may involve stimulating cultured primary human keratinocytes with selected cytokines followed by examineing induced responses using gene chips, qRT-PCR and Western blots for markers associated with a pruritus signature. As another example, since activation of certain G-protein coupled receptors or transient receptor potential channels by specific pruritogens is critical for signal transduction in itch, we are interested in deciphering the specific role of the relevant receptors and channels. As a third example, the student may have the opportunity to assist us in the use of 2-photon in vivo confocal microscopy of an atopic dermatitis model in Brainbow mice to visualize the changes in the architecture of cutaneous sensory nerves. Last, there are several clinical studies that can be approached, these include the itch associated with burns, and the use of Fraxel laser or cold to treat itch. Increased nerve fiber density has been described in humans with, and mouse models of, atopic dermatitis. The traditional view is that these neural changes are reactive to ongoing inflammation or scratching. I will present data that challenges the traditional view. We find that neural recruitment and activation are required, and provide a scaffold, for the elaboration and maintenance of the inflammatory cascade in allergic eczema. We further implicate a class of orphan receptor in this process.