2008 : Paul Khavari M.D., Ph.D., Stanford, USA
For the past 2 decades, Professor Paul Khavari has studied epidermal homeostasis and neoplasia. With his laboratory in Stanford, he contributed to the understanding of the role of different proteins implied in proliferative self-renewal and terminal differentiation of human epidermal tissue. Currently, his laboratory is pursuing its research in order to characterize the mechanisms controlling the transition from epidermal stem cells to differentiated cell in a physiologic manner, as well as to develop new molecular therapeutics for the treatment of skin and systemic disease.
2007: Richard L. Gallo M.D.,Ph.D., San Diego, USA .
More than ten years ago, Professor Gallo and his colleagues discovered that, following injury, the skin can produce peptides with antibiotic activity. This finding led to the characterization of cathelicidins as distinct natural antimicrobials in normal skin and in skin disorders. Professor Richard Gallo’s team has found that in patients with atopic dermatitis a lack of expression of cathelicidins and defensins is correlated with their susceptibility to infection. “This observation explains in part why atopic dermatitis patients are more susceptible to certain skin infections. Ongoing work in the laboratory is attempting to explain why this occurs; it is primarily a problem with regulation of gene expression rather than a defect in the gene itself. We have recently discovered that the metabolic activation of vitamin D leads to appropriate expression of antimicrobial peptides and pattern recognition receptors such as TLR2,” explained Professor Gallo. He plans to use the Award, worth 40,000 €, on a project to identify antimicrobial peptides produced by S. epidermidis, a bacterium which colonizes normal skin and which protects the skin from infection with pathogenic group A streptococci. He also aims to investigate how S. epidermidis influences the antimicrobial and cytokine response in keratinocytes.   “Our most recent work has defined how specific elements of the normal skin microflora influence the innate immune barrier of the skin. These interactions conclusively show the symbiotic relationship between commensal bacteria and keratinocyte immune function,” said Professor Gallo.
2006: Irwin McLean Ph.D., DSc, FRSE, Professor of Human Genetics, University of Dundee, Scotland, UK, for his pioneering research into the role of filaggrin gene mutations in ichthyosis vulgaris and atopic eczema.
Filaggrin is one of a cluster of seven large genes of the fused S100 class within the 1q21 locus. The other genes are filaggrin-2, trichohyalin, trichohyalin-like 1, cornulin, repetin and hornerin. He plans to use the Award, worth 40,000 €, to carry out an analysis of fused S100 genes in ichthyosis vulgaris (a hereditary tendency to dry scaling skin) and atopic eczema (an intensely itchy skin disease associated with allergies). The recent discovery by Professor McLean's team that filaggrin gene mutations cause ichthyosis vulgaris, and are very strong predisposing factors for atopic eczema, has taken them from the study of rare conditions, affecting a few tens of thousands of patients, to diseases affecting many tens of millions worldwide.
2005: Masayuki AMAGAI, M.D. Ph.D., Professor of Dermatology and Chairman of the Department of Dermatology. Keio University School of Medicine, Tokyo, Japan, for his research project on peripheral tolerance mechanisms in the skin.
Professor Amagai’s past research includes pioneering studies on the mechanisms which underly pemphigus vulgaris, a life threatening disease manifested by skin blisters. He and his colleagues have previously cloned the pemphigus vulgaris antigen and demonstrated that the autoimmune disease pemphigus is caused by antibodies directed against desmoglein 3, a protein which is crucial for the cell to cell adhesion of epidermal keratinocytes. For his current project Prof. Amagai and his team will investigate the cellular and molecular mechanisms preventing that cells of the immune system from attacking autoantigens in healthy skin. “Understanding the precise mechanism of peripheral tolerance in skin is crucial for the development of novel ways to maintain healthy skin and avoid autoimmune diseases such as pemphigus,” explained Professor Amagai.
2004: Thomas SCHWARZ, M.D. University of Kiel, Germany Columbia University, New York, USA Project: Research into the molecular mechanisms of immunosuppression induced by ultraviolet radiation
Professor Thomas Schwarz, one of Germany's leading dermatologists, has made numerous contributions to our understanding of UV effects on normal skin, particularly the mechanisms by which UV modulates immune reactions and induces apoptosis (programmed cell death) of damaged cells. His recent observation that one of the immunomodulatory cytokines released after UV exposure, interleukin-12, can prevent UV-induced apoptosis, and does so at least in part by enhancing repair of UV-induced DNA damage, is most intriguing and ties together two types of UV responses previously thought to be quite independent of each other.
2003: Angela M. Christiano, Ph.D. Columbia University, New York, USA Project: Research into epidermal biology.
The Award will be utilised for Dr Christiano's proposed research project to explore the molecular mechanisms of epidermal growth and differentiation. Her contributions range from breakthrough findings in hair development to major advances in extracellular matrix biology and they have added tremendously to the advancement of our understanding of skin biology. Her continuing commitments have established her laboratory as a focal point for cutting edge skin research.
2002: Dennis R. Roop, Ph.D. Center for Cutaneous Molecular Biology, Baylor College of Medicine, Houston, USA Project: The role of p63 in epidermal development.
The p53/65/73 family of proteins plays a key role in the suppression of tumors and in embryonic development. Dr. Roop's work has helped to establish the role of these proteins during tissue homeostasis and in particular for keratinocyte differentiation. His current work focuses on the molecular regulation of p63, a member of this family, and will help to elucidate its contribution to the formation of an intact epidermal barrier.
2001: Fiona M. Watt, D.Phil. Keratinocyte Laboratory, Imperial Cancer Research Fund, London, UK Project: Research on keratinocyte biology
Dr Watt's research contributes to the understanding of cell differentiation in the epidermis. Dr Watt's work on keratinocyte differentiation and on epithelial stem cells has been groundbreaking and it has considerably advanced the understanding of the function of normal skin and inspired many skin researchers within and outside dermatology. This project will further define the ways in which keratinocytes mature and will ultimately contribute to improved care of healthy skin.
2000: Michael Karin, Ph.D. Laboratory of Gene Regulation and Signal Transduction, School of Medicine, University of California, San Diego, USA Project: Examination of the role of the IKKgamma.NEMO gene in regulating skin differentiation.

Michael Karin's research has contributed greatly to the understanding of gene regulation in general and has had an huge imapct on dermatological
research over the past 2 decades. He has characterised various proteins, which play a central role in the regulation of gene transcription and thereby has advanced the understanding of differentiation of skin cells as well as their reaction to environmental factors such as UV irradiation.Dr Karin's current work indicates that the elements controlled by the transcription factor NF-KappaB are the heart of the regulation of cell proliferation, apoptosis and Inflammatory processes which regulate the physiology of the epidermis and allow it to adapt to external factors.

1999: Jonathan Rees, M.D. University of Edinburgh, Edinburgh, UK Project: Towards a quantitative genetic model of the interaction of ultraviolet radiation and skin.

The recent studies of Professor Rees have enabled the cloning of the melanocortin 1 receptor gene and shown that variants of this gene are associated with different types of skin, in particular the red phenotype and the risk of melanoma. The work demonstrates that small differences in a single gene can determine both the appearance and the physiological behaviour of healthy skin.This is the first step towards a molecular model of different healthy skin types and their respective sensitivity to external aggressions. The research represents a major advance in preventive medicine and skin physiology and these type of studies will ultimately lead to a classification of healthy skin based on the knowledge of molecular skin properties.
Professor Rees' future project is to find a quantitative genetic model of the interaction of ultraviolet radiation and skin. The results of this research, which should further our understanding of the skin's reaction to UV radiation, are expected to have implications in the fields of both dermatology and cosmetic research.

1998: Jean Krutmann, M.D. Heinrich Heine University, Düsseldorf, Germany Project: Research into the role of ceramides in UV-A radiation-induced signal transduction in human skin cells.

Professor Krutmann's photobiological research has been key in revealing both the harmful and therapeutic effects of UV-A light through the study of its intracellular effects in the skin. His current project is set to further investigate the effects of UV-A light on signalling in skin cells by focusing on the role of intracellular ceramides in this process.
Recently it was discovered that certain ceramides - lipids which are essential to the maintenance of the permeability of the stratum corneum - were capable of modulating gene expression in human epidermis. Professor Krutmann's project aims to understand the consequences of the liberation of ceramides by UV-A in human epidermis.
The studies will help to better understand the action as well as the possible side effects of UV-A irradiation. Indeed, this research should lead to vital information in the mechanism of skin cancer formation following UV-A aggression and in the understanding of the mechanisms whereby skin ageing is accelerated by the action of UV-A. It should also enable us to learn how the use UV-A to treat certain skin diseases.

1997: Jens-Michael Schröder, Ph.D. Christian-Albrechts University, Kiel, Germany Project: Research into the regulation of the production of antimicrobial peptides in the epidermis.

It is known that peptide antibiotics are present in vertebrate skin, trachea and tongue epithelia. The research carried out shows the presence of such antimicrobial peptides in human skin. The research, which isolated antimicrobial peptides from psoriatic scales, resulted in the finding of a form of human b -Defensin, named hb D-2. This peptide is regulated in response to contact with micro-organisms and was found to kill certain bacteria and yeasts.
Prof. Schröder's research will continue to look at hb D-2 in the skin as well as other antimicrobial proteins in order to check whether the latter are present in healthy skin and, if so, whether they are regulated by micro-organisms. The research will also look at other antimicrobial peptides isolated from psoriatic scales.
This research project aims to further the understanding of healthy skin to fight against bacteria and fungi, find new answers to why healthy skin is free of infection and form ideas of how to help skin produce antimicrobial peptides in order to form a defence against micro-organisms.

1996: Akira Takashima, M.D., Ph.D. University of Texas Southwestern Medical Center, USA Project: Research into the molecular basis for Langerhans cell-specific transcription of the Dectin-1 gene.

The ability to study the biology of antigen-presenting cells at the molecular level has become possible through the development of several cell lines, including the XS lines developed at the Southwestern Medical Center. This has in turn enabled researchers to clone unique genes that are expressed by antigen-presenting cells of the skin, i.e. Langerhans cells, identify the cytokines produced by Langerhans cells, and modulate their function genetically by introducing selected genes.
The research project focuses on studying the structure and function of dectin-1, one of two unique molecules which have been identified at the Southwestern Medical Center. They are transmembrane glycoproteins expressed selectively by Langerhans cells and on their surfaces. Observations suggest that dectin-1 may function as 'co-stimulatory molecules', facilitating the activation of T cells.
The project is researching the molecular mechanisms by which the transcription of the dectin-1 gene is controlled in Langerhans cells. The studies will provide new insights into the biology of Langerhans cells and form technical and conceptual bases for the future development of Langerhans cell-targeted genetic vaccines.