Article
A common form of dominant human IFNAR1 deficiency impairs IFN-α and -ω but not IFN-β-dependent immunity.
The Journal of experimental medicine - 3 Feb 2025
Al Qureshah Fahd, Le Pen Jérémie, de Weerd Nicole A, Moncada-Velez Marcela, Materna Marie, Lin Daniel C, Milisavljevic Baptiste, Vianna Fernanda, Bizien Lucy, Lorenzo Lazaro, Lecuit Marc, Pommier Jean-David, Keles Sevgi, Ozcelik Tayfun, Pedraza-Sanchez Sigifredo, de Prost Nicolas, El Zein Loubna, Hammoud Hassan, Ng Lisa F P, Halwani Rabih, Saheb Sharif-Askari Narjes, Lau Yu Lung, Tam Anthony R, Singh Neha, Bhattad Sagar, Berkun Yackov, Chantratita Wasun, Aguilar-López Raúl, Shahrooei Mohammad, Abel Laurent, Bastard Paul, Jouanguy Emmanuelle, Béziat Vivien, Zhang Peng, Rice Charles M, Cobat Aurélie, Zhang Shen-Ying, Hertzog Paul J, Casanova Jean-Laurent, Zhang Qian
Abstract excerpt
Autosomal recessive deficiency of the IFNAR1 or IFNAR2 chain of the human type I IFN receptor abolishes cellular responses to IFN-α, -β, and -ω, underlies severe viral diseases, and is globally very rare, except for IFNAR1 and IFNAR2 deficiency in Western Polynesia and the Arctic, respectively. We report 11 human IFNAR1 alleles, the products of which impair but do not abolish responses to IFN-α and -ω without...
Topics
Join the communities discussing this publication.