17 octobre 2024: Pr Russell E. Vance
12H30
CMU - AUDITOIRE MÜLLER (A250)
suivi d'un apéritif
Hôte: Pr Cem GABAY
Centre de recherche sur l'inflammation de Genève
Département de médecine, Faculté de médecine UNIGE
PROF. RusselL E. Vance
Professor and HHMI Investigator
Department of Molecular and Cell Biology, University of California, Berkeley
«Tuberculosis as an interferonopathy»
Tuberculosis is caused by Mycobacterium tuberculosis, a bacterium that accounts for more human mortality than any other. Despite being identified more than 140 years ago, we lack a clear understanding of TB pathogenesis, and unfortunately, the mechanisms employed by M. tuberculosis to become the world’s most successful bacterial pathogen remain obscure. In this lecture, Russell Vance will discuss the emerging view that tuberculosis can be considered a type of interferonopathy—a disease driven by type I interferons. Conventional interferonopathies are autoinflammatory diseases, without an infectious etiology, whereas tuberculosis is caused by a bacterium. Nevertheless, there may be some similarities between these two disease states. In both cases, type I interferons orchestrate an underlying state of immunosuppression that paradoxically co-exists with overt inflammation. Under this view, the fundamental virulence strategy of M. tuberculosis is to be intrinsically resistant to the inflammatory response while exploiting the underlying immunosuppression. The hope is that conceiving tuberculosis as an unconventional interferonopathy may suggest fruitful avenues for therapeutic intervention.
Biography
Russell Vance grew up in Canada where he attended Queen’s University in Kingston, Ontario for his undergraduate (Biochemistry) and Master’s (Philosophy of Science) degrees. He obtained his PhD in Immunology from the University of California, Berkeley, under the mentorship of David Raulet. His postdoctoral work was with John Mekalanos and William Dietrich at Harvard Medical School. Since establishing his lab at UC Berkeley in 2006, Vance has been interested in identifying the molecular mechanisms underlying innate immune recognition of bacterial pathogens. His lab is known primarily for its studies of Legionella pneumophila, as well as for mechanistic work on inflammasomes and the discovery that cyclic-di-nucleotides are direct agonists of STING. Since 2013, Vance has been an Investigator of the Howard Hughes Medical Institute. He is also a Fellow of the American Academy of Microbiology. In 2020, he was awarded the William B. Coley Award for Basic and Cancer Immunology by the Cancer Research Institute. Most recently, the Vance Lab has turned its focus to two bacterial pathogens with a significant global burden, Shigella flexneri and Mycobacterium tuberculosis.
2 juil. 2024