Awards for Hammad Hassan, Alina Neunkirchner and Klaus Schmetterer
The Austrian Society of Allergology and Immunology awarded
Dr. Hammad Hassan the Karl Landsteiner Prize for tremendous work in the field of immunological basic research,
Mag Alina Neunkirchner the Clemens von Pirquet Award for tremendous work in the field of allergological research and
Mag DDr. Klaus Schmetterer the Dissertation Award for dissertations with excellent scientific content in the field of Immunology /Allergology
Dr. Hammad Hassan
His work entitled "Cd8 enhancer E8I and Runx factors regulate CD8α expression in activated CD8+ T cell" has been published in the Journal of Proceedings of the National Academy of Sciences (PNAS) in 2011. In this study, he has identified a novel transcriptional program where Cd8 enhancer E8I and Runx3/CBFβ complexes regulate Cd8α expression during effector T cell differentiation. The data suggest a differential mechanism of how CD8 expression is regulated in naive and effector T cells and might be important to investigate the (patho)physiological conditions under which wild-type CD8+ T cells down-regulate CD8α expression via modulation of E8I enhancer (or Runx/CBFβ activity).
To his person
He was born in 1979 Mardan, Pakistan and did his Master studies in Biochemistry from the Institute of Chemical Sciences, University of Peshawar, KPK, Pakistan. He got UGC fellowship for Master of Philosophy. His research focus was to study the genetic variations of β-thalassemia in Pakistani population. Then he received a PhD fellowship from the Government of Pakistan (Higher Education Commission of Pakistan) and joined the group of Prof. Dr. Wilfried Ellmeier at the Institute of Immunology, Medical University of Vienna. He finished his PhD study in 2011. Currently he is working as a post-doctoral fellow.
Mag. Alina Neunkirchner
In her publication Human TCR tg Bet v 1-specific Th1 cells suppress the effector function of Bet v 1-specific Th2 cells Alina Neunkirchner, MSc. (Institute of Immunology, group: ao.Univ.Prof. Dr. Winfried Pickl) describes the characterization of a human Bet v 1-specific T cell receptor (TCR) recognizing the immunodominant T cell epitope Bet v 1142-153. Transfer of the Bet v 1-specific TCR alpha and beta chains into human peripheral blood T cells generates TCR transgenic T cells that resemble the original T cell clone in its fine specificity. Furthermore the authors show that polarization of TCR transgenic T cells with the help of artificial antigen-presenting cells (aAPC) expressing membrane-bound human interleukin-12 strictly induced Th1-polarized TCR transgenic T cells. In co-culture experiments these TCR transgenic Th1 cells potently suppress the effector function of Bet v 1-specific Th2 cells upon allergen-specific re-stimulation. These important novel insights were published as a featured article in the Journal of Immunology.
In his thesis “Modulation of allergen-specific T-cell responses using novel antigen-presenting platforms and transgenic regulatory T-cells” Klaus Schmetterer, MD, PhD (Institute of Immunology, group: ao.Univ.Prof. Dr. Winfried Pickl) describes the establishment of novel innovative strategies to modulate allergen-specific T-cell responses and assessment of these approaches in vitro. In the key publication of his PhD thesis Klaus Schmetterer describes the transgenic generation of allergen-specific regulatory T-cells by the retroviral co-introduction of a birch pollen allergen Bet v 1-specific T-cell receptor in concert with the human FOXP3 gene. The suppressive function of these transgenic regulatory T-cells is strictly dependent on activation by the cognate antigen (i.e. the allergen Bet v 1). This work was published as a featured article in a special edition of the Journal of Allergy and Clinical Immunology. Since April 2012 Klaus Schmetterer is working as a resident at the Department for Laboratory Medicine (Head: Univ.-Prof. Dr. Oswald Wagner) at the Medical University of Vienna. He is continuing to study T-cell regulatory processes in co-operation with ao.Univ.Prof. Dr. Winfried Pickl.
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