JRG: An immunogenetic approach to unravel adaptive immune defects in human systemic autoinflammatory diseases
Hirotsugu Oda
CECAD, University of Cologne
Contact: hoda(at)uni-koeln.de
For more information please visit: Oda Lab
Abstract
Systemic Autoinflammatory Diseases (SAIDs) are a group of human disorders characterized by genetic hyperactivation of innate immunity, resulting in intractable inflammatory manifestations such as prolonged fever, rash, arthritis and colitis. Currently the clinical outcome of SAIDs is still discouraging, and there is an urgent need to discover new molecular targeted therapies. We will use a transdisciplinary approach by combining our experiences in clinical medicine, human genetics, bioinformatics and molecular immunology, to elucidate the contribution of cell death dysregulations as an important underlying pathomechanism of human SAIDs.
Project related Publications
Lalaoui N*, Boyden SE*, Oda H*, Wood GM, Stone DL, Chau D, Liu L, Stoffels M, Kratina T, Lawlor KE, Zaal KJM, Hoffmann PM, Etemadi N, Shield-Artin K, Biben C, Li Tsai W , Blake MD, Kuehn HS, Yang D, Anderton H, Silke N, Wachsmuth L, Zheng LL, Sampaio Moura N, Beck DB, Gutierrez-Cruz G, Ombrello AK, Pinto-Patarroyo GP, Kueh AJ, Herold MJ, Hall C, Wang H, Chae JJ, Dmitrieva NI, MacKenzie M, Light A, Barham BK, Jones A, Romeo TM, Zhou Q, Aksentijevich I, Mullikin JC, Gross AJ, Shum AK, Hawkins ED, Masters S, Lenardo MJ, Boehm M, Rosenzweig SD, Pasparakis M, Voss AK, Gadina M, Kastner DL, Silke J (*equal contribution). Mutations that prevent caspase cleavage of RIPK1 cause autoinflammatory disease. Nature, volume 577, pages103–108(2020).