Prize Winners 2013

Technical University and Helmholtz Center, Munich (Germany)

Dr. Eyerich's research activity focuses on<strong> deciphering Th subsets and function in skin inflammatory and allergic diseases. The subsets are defined according to their production of lineage-type cytokines and functions. Dr. Eyerich has identified a new subset of human Th cells that infiltrate the epidermis in individuals with inflammatory skin disorders and is characterized by the secretion of IL-22 and TNF-alpha, but not IFN-gamma, IL-4, or IL-17. Dr. Eyerich's other scientific achievements include the identification of the role for Th17 cytokines in skin immunity in the orphan disease chronic mucocutaneous candidiasis, as well as in atopic eczema, the proof of a causative role for T cells in atopic eczema and for the in vivo relevance of the cutaneous T cell composition in atopic eczema patients, and the description of the functional impact of T cell cytokines on epithelial cells in allergic asthma.

Dr. Eyerich has become a leading scientist in the field of T helper cell communication in skin allergic diseases such as psoriasis or atopic eczema. Her scientific contributions have brought the field of allergy research enormously forward, and her findings will help to develop new therapeutic strategies for these socioeconomic-relevant diseases.

Institute Curie, Paris (France)

During his Ph.D. studies, he identified the receptor for the human T cell leukemia virus envelope, GLUT1 (Cell). He then contributed to showing that this protein is expressed by a thymocyte subset and that GLUT-1 is a transporter of vitamin C in red blood cells. During his postdoctoral work, Dr. Manel demonstrated that RORᵧT is necessary for the production of IL17 and that HIV infection leads to a specific perturbation in Th17. In mice, he contributed to the demonstration that a single bacteria, the segmented filamentous bacteria, is sufficient for Th17 induction in the gut. More recently, Dr. Manel’s research interests have focused on the infection of dendritic cells (DC) by HIV1 and HIV2.

The natural history of HIV-2 infection tends to be more benign than that of HIV-1, and most patients infected solely with HIV-2 do not progress to AIDS. Previous research suggests that HIV-2 infection protects against subsequent HIV-1 infection and, in cases of dual infection, slows the rate of HIV-1 disease progression. Dendritic cells are main actors in the generation of protective adaptive immune responses, and Dr. Manel was the first to describe a cell-intrinsic cryptic sensor in DC that recognizes the viral capsid and protects the cells from HIV1 infection. On the other hand,he described a viral variant of HIV2 able to activate DC, thereby inducing a strong stimulation of HIV-specific CD8 T cells. His continued work will undoubtedly generate important data in the design of an HIV-1 vaccine.

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Final Report

University of Bern (Switzerland)

At a scientific level, Dr. Eggel is involved in the discovery of<strong> novel strategies to prevent allergic hypersensitivity reactions using disruptive IgE inhibitors. Using cutting edge technology, namely a novel platform of non-immunoglobulin binding molecules termed Designed Ankyrin Repeat Proteins (DARPins), he identified novel inhibitory compounds of allergic hypersensitivity reactions. He recently completed an outstanding study that he initiated during his Ph.Dd thesis work, which revealed a novel class of disruptive IgE inhibitors that could potentially revolutionize allergy drug development and therapy.

Binding of IgE to FcεRI is considered to be a central event in the development of a type I allergy. In collaboration with Prof. Theodore Jardetzky’s group at Stanford University, Dr. Eggel identified and characterized a novel mechanism to remove IgE, i.e., a key-player in the allergic reaction, from its high affinity receptor (FcεRI). Therefore, the disruption of this high-affinity interaction using novel IgE inhibitors might represent a remarkable novel strategy to block allergic reactions.