Dr. Sergei Grando is Professor of Dermatology. He graduated in 1980 from Kiev Medical Institute, Ukraine, completed residency in Dermatology and Venereology at Kiev Postgraduate Institute for Physicians and then became a faculty member. He obtained his Ph.D. in 1984 for studies of atopic dermatitis and then, in 1989, the Doctor of Science in medicine (D.Sci.) for studies of pemphigus and pemphigoid. From 1991 to 1996 he was on faculty at University of Minnesota, from 1996 to 2007 at University of California Davis, and then joined Department of Dermatology of University of California Irvine. He is certified by the American Board of Dermatology. Dr. Grando has published more than 270 articles or monographs, obtained several research grants from National Institutes of Health, and many other granting agencies. He is a Vice Chair of Medical Advisory Board of International Pemphigus & Pemphigoid Foundation and a member several international and national professional societies and advisory groups. He was awarded as a Doctor of the Year by International Pemphigus & Pemphigoid Foundation.
Dr. Grando is a leading expert and researcher in autoimmune blistering diseases. Dr. Grando utilized pemphigus patients' IgGs as a probe to identify the pathophysiologically relevant target antigens in the autoimmune blistering disease pemphigus. He found, unexpectedly, that autoantibodies targeted several known as well as novel members of the acetylcholine (ACh) receptor gene superfamilies expressed by skin cells. Later, he has now demonstrated that these receptors control cell shape and intercellular adhesion, and their blockade by auto-antibodies produces cell dysadhesion and blisters. Dr. Grando's lab demonstrated that pemphigus vulgaris IgG and methylprednisolone exhibit reciprocal effects on keratinocyte adhesion molecules. He discovered novel mechanisms of targeting cell death and survival and therapeutic action of intravenous IgG (IVIg) in pemphigus. The results indicate that in different pemphigus patients, IgG-induced acantholysis proceeds predominantly via distinct, yet complementary, pathways of programmed cell death and that IVIg protect target cells by up-regulating endogenous caspase and calpain inhibitors. The results of his work have altered the way physicians throughout the world understand the mechanisms of pemphigus.