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Profil
| Derzeitige Stellung | Professor W-2 und Äquivalente |
|---|---|
| Fachgebiet | Immunologie,Klinische Neurologie; Neurochirurgie und Neuroradiologie |
| Keywords | MS, EAE, Immunotherapy, Autoimmunity, Central nervous system |
Aktuelle Kontaktadresse
| Land | Israel |
|---|---|
| Ort | Rehovot |
| Universität/Institution | Weizmann Institute of Science |
| Institut/Abteilung | Department of Immunology |
Gastgeber*innen während der Förderung
| Prof. Dr. Hartmut Wekerle | Abteilung Neuroimmunologie, Max-Planck-Institut für biologische Intelligenz, Planegg-Martinsried |
|---|---|
| Beginn der ersten Förderung | 01.06.2007 |
Programm(e)
| 2006 | Forschungspreis-Programm auf Gegenseitigkeit für Wissenschaftler*innen aus dem Ausland |
|---|
Projektbeschreibung der*des Nominierenden
| Dr. Avraham Ben-Nun is one of the leading neuroimmunologists internationally. His contributions have imprinted our concepts of the pathogenesis of multiple sclerosis and of other organ specific autoimmune diseases. Dr. Ben-Nun made his entry into science with a path-breaking discovery. As a young PhD student sharing his time between the Weizmann Institute and the Max-Planck-Institute of Immunobiology Freiburg he was centrally involved in the development of a novel technology, which allowed for the first time the isolation and propagation of autoreactive, autoaggressive T cell lines. This approach then led to the first formal demonstration of autoimmune T cells in the healthy immune repertoire, a discovery, which changed the central concept of immune reactivity and, implicitly, our understanding of autoimmune disease. After a post-doctoral period spent at Harvard Medical School, which introduced him into the then young field of molecular immunology, Dr. Ben-Nun returned to his home institution, the Weizmann Institute, where he built up an independent research group. Avraham Ben-Nun redirected his interest to two main issues, the importance of microbial structures in modulating autoimmune reactions, and the autoimmune response against a particular myelin component, the Myelin Oligodendrocyte Glycoprotein (MOG). He was one of the first to show that, contrary to intuition, microbial products, such as the staphylococcal enterotoxins, heat shock proteins and pertussis toxins may exert beneficial effects on the unfolding myelin-targeted autoimmune response. He furthered that much of this protective activity is exerted by particular regulatory T lymphocytes that oppose the generation of autoaggressive immune cells. Debatably even more visible has been Dr. Ben-Nun's "second leg", his work on immune reactivity against MOG, today one of the most prominent candidate autoantigens in human MS. His group was the first to show that indeed in human MS patients the cellular anti-MOG response is higher than in matched healthy persons. He uses this finding currently to design new and autoantigen specific therapies of human disease. A real blockbuster was his identification of MOG peptide 35-55 as an encephalitogenic autoantigen in the C57BL mouse. This discovery allowed for the first time the predictable induction of EAE in "black" mice, which before were reputed to resist any attempts of autoimmunization. Given that most transgenic mice are being breed on C57BL or on H-2b identical 129/J backgrounds, Ben-Nun's finding opened a completely new avenue to study (CNS) autoimmunity in available transgenic mice. Dr. Ben-Nun will now use his Humboldt Prize to deepen his existent cooperation with the Department of Neuroimmunology (MPI Neurobiology, Martinsried). The two partners plan to use new experimental models of spontaneous myelin autoimmune disease, which had been developed in Martinsried, to validate possible therapeutic effects of Ben-Nun's new immunotherapeutic drugs. The drugs will be tested at different time points before and during spontaneous EAE. There will be particular attention to determinant spreading events that may or may not be affected by the treatments. This cooperation hopefully will help design a new, specific treatment of brain autoimmunity, such as Multiple Sclerosis. |