EAACI-Allergopharma Research Award
Allergopharma Award, EAACI Executive Committee
With the EAACI-Allergopharma Research Award, we want to acknowledge talented young researchers and motivate them to drive innovation in the field of allergy research.
The award was established in 2000, on the initiative of Allergopharma, in collaboration with the European Academy of Allergy and Clinical Immunology. It is intended that the Award should recognize the scientific achievements of young scientists working in the field of allergy and encourage their engagement in further research.
It is open to members of the EAACI and, in particular, to Junior Members, who have conducted their research in an European centre. An application for consideration for the Award shall take the form of a full research paper published in an international peer reviewed journal in the last three years, together with a cover letter detailing the extent of the applicant’s contribution to the research and a curriculum vitae including a full list of publications.
The applications will be considered by an ad hoc commission nominated by the EAACI Executive Committee and should be submitted electronically to both the EAACI Headquarters (email@example.com). The research paper, curriculum vitae and a covering letter should be included as three separate attachments. If this is not possible, then postal applications can be sent to EAACI Headquarters, Hagenholzstrasse 111, 3rd Floor, 8050 Zurich, Switzerland (Tel.: +41 44 205 55 33).
Please see the official announcement for the Allergopharma Award on the right hand side for this years deadline for submission.
Previous winners of the Allergopharma Award:
Dr. Flore Amat
Epidémiologie des Maladies Allergiques et Respiratoires, France
Project: Risk factors for asthma at school age in children with early-onset atopic dermatitis
Dr Brecht Steelant
KU Leuven, Leuven, Belgium
Project: Role of the epithelial barrier in the pathophysiology of allergic rhinitis
Kristina Johansson, Krefting Research Centre, University of Gothenburg, Sweden
MicroRNA-155 is a critical regulator of type 2 innate lymphoid cells and IL-33 signaling in experimental models of allergic airway inflammation
J Allergy Clin Immunol. 2017 Mar; 139(3): 1007-1016
Dr. Irisz Karolina Levai, University of Kent, Great Britain
Dr. Alexander Eggel, University Hospital Bern, Switzerland
Accelerated dissociation of IgE-F&RI complexes by disruptive inhibitors actively desensitizes allergic effector cells
J Allergy Clin Immunol. 2014 Jun; 133(6): 1709-1719
Prof. Dr. Natalija Novak, University of Bonn, Germany
Early suppression of basophil activation during allergen-specific immunotherapy by histamine receptor 2. J Allergy Clin Immunol. 2012 Nov;130(5):1153-1158
Dr. rer. physiol. Christian Möbs, Philipps-Universität Marburg, Germany
Birch pollen immunotherapy results in long-term loss of Bet v 1-specific TH2 responses, transient TR1 activation, and synthesis of IgE-blocking antibodies. J Allergy Clin Immunol 2012;130:1108-16.
Dr. Oscar Palomares Gracia, PhD, School of chemistry Ciuadad Universitaria s/n, Madrid, Spain
Induction and maintenance of allergen-specific FOXp3+ Treg cells in human tonsils as potential first-line organs of oral tolerance. J Allergy Clin Immunol. 2011; 10.1016/2011.09.031.
Denis Bedoret, DVM, PhD - Children's Hospital Boston, Boston, USA
Lung interstitial macrophages alter dendritic cell functions to prevent airway allergy in mice. J. Clin. Invest. 2009: 119:3723–3738.
Jorge Esparza-Cordillo, PhD – MDC for Molecular Medicine, Berlin, Germany und
Stephan Weidinger, MD - Technische Universität München – Munich, Germany
A common variant on chromosome 11q13 is associated with atopic dermatitis.
Nature Genetics 2009;41:596-601.
PD Dr. Marco Idzko, - COPD & Asthma Research-Group ,University Hospital Freiburg, Freiburg, Germany
Extracellular ATP triggers and maintains asthmatic airway inflammation by activating dendritic cells. Nature Medicine, 2007;13/8:913-919.
Dr. Georgina Xanthou, Biomedical Research Foundation, Academy of Athens (BRFAA), Athens, Greece
Ostepontin has a crucial role in allergic airway disease through regulation of dendritic cell subsets. Nature Medicine 2007; 13/5:570-578.
Dr. rer. nat. Carsten B. Schmidt-Weber, SIAF, Davos, Switzerland
Molecular mechanisms underlying FOXP3 induction in human T cells. The Journal of Immunology, 2006;176:3593-3602.
PD Dr. med. Claudia Traidl-Hoffmann, TU München; München, Germany.
Pollen associated phytoprostanes inhibit dendritic cell interleukin-12 production and augument T helper type 2 cell polarization. JEM 2005;201/4:627-635.
Univ.Doz. Dr. Barbara Bohle, AKH, University of Vienna, Vienna, Austria.
A novel approach in specific allergy treatment: The recombinant fusion protein of a bacterial cell surface (S-Layer) protein and the major birch pollen allergen Bet v 1 (rSbsC-Bet v 1) combines reduced allergenicity with immunomodulating capacity.The Journal of Immunology 2004;172:6642-48.
Dr. Hamida Hammad, Erasmus Medical Centre, Rotterdam, The Netherlands.
Essential role of lung plasmacytoid dendritic cells in preventing asthmatic reactions to harmless inhaled antigen. J. Exp. Med. 2004;200:89-98.
Professor Eckard H. Hamelmann, MD, Humboldt-University Berlin, Berlin, Germany. Exposure to endotoxin and allergen in early life and its effect on allergen sensitization in mice. J. Allergy Clin. Immunol. 2003;112:389-396.
Dr. Eleanor Ling, Imperial College Faculty of Medicine, London, UK.
CD4+CD25+ regulatory T cell suppression of allergen-driven T cell activation is related to atopic status and expression of allergic disease. The Lancet 2004;363/9409:608-615.
Dr. Peter W. Hellings, University Hospital Gasthuisberg, Leuven, Belgium.
Blockade of CTLA-4 enhances allergic sensitization and eosinophilic airway inflammation in genetically predisposed mice. Eur. J. Immunol 2002;32:585-594.
Dr. Susanne Vrtala, AKH, University of Vienna, Vienna, Austria.
Genetic engineering of a hypoallergenic trimer of the major birch pollen allergen,
Bet v 1. FASEB J. 2001;15:2045-2047.
Professor Cezmi A. Akdis, MD, SIAF, Davos, Switzerland.
A molecular basis for T cell suppression by IL-10: CD28- associated IL-10 receptor inhibits CD28 tyrosine phosphorylation and phosphatidylinositol 3-kinase binding. FASEB J. 2000;14:1666-1668.