High expression of interleukin-18 receptor alpha correlates with severe respiratory viral disease and defines T cells with reduced cytotoxic signatures

白细胞介素-18受体α的高表达与严重的呼吸道病毒疾病相关,并定义了细胞毒性特征降低的T细胞。

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作者:Aira F Cabug,Jeremy Chase Crawford,Hayley A McQuilten,Isabelle J H Foo,Lilith F Allen,Deborah Gebregzabher,Robert C Mettelman,Tanya Novak,Janet Chou,Louise C Rowntree,Ruth R Hagen,Abby J Thomson,Genevieve E Martin,Brad Gilbertson,Michael Nt Souter,Fiona James,Emma Goodall,Simone Rizzetto,Tim Flerlage,Xiaoxiao Jia,Lee-Ann Van de Velde,So Young Chang,Fabio Luciani,Ryan S Thwaites,Jason A Trubiano ,Tom C Kotsimbos,Allen C Cheng,Adrienne G Randolph,Paul G Thomas,Jianqing Xu,Zhongfang Wang,Thi H O Nguyen #,Brendon Y Chua #,Lukasz Kedzierski #,Katherine Kedzierska #

Abstract

Hyperactivated immunity underpins severe outcomes of respiratory viral infections, yet specific immune perturbations are ill-defined. Our recent findings identified OLAH (oleoyl-ACP-hydrolase) as a driver of life-threatening viral diseases. In the same patient cohorts, we now identify the gene encoding IL-18Rα chain (IL18R1), as being highly expressed in life-threatening influenza, COVID-19, RSV and multisystem inflammatory syndrome in children (MIS-C) and demonstrate markedly elevated surface protein IL-18Rα expression on CD8 T cells in these infections. Using a mouse model of severe influenza, we further show that high IL-18Rα expression on effector T cells is associated with increased disease severity. We find that IL-18Rα expression on CD8 T cells is inversely associated with cytotoxicity-related genes, including granzyme A, granzyme B, perforin, Eomes, and KLRG-1. Our study demonstrates that IL-18Rα is associated with severe and fatal respiratory disease outcomes and proposes the use of IL-18Rα as a potential biomarker for severe respiratory viral disease.

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