Barbara A Malynn

Correction to: Nature Immunology https://doi.org/10.1038/s41590-020-0634-4, published online 16 March 2020. In the version of the article initially published, in Fig. 2, there were duplicate FACS plots in panels d and e. Fig. 2 has now been updated with the correct data, as seen in Fig. 1 below. This correction has been made to the HTML and PDF versions of the article. Fig. 1 Original and corrected Fig. 2d,e. About this article Razani, B., Whang, M.I., Kim, F.S. et al.

Conghui Cao, Xue Fu and Xiaoli Wang* Department of Endocrinology and Metabolism, Institute of Endocrinology, National Health Commission (NHC) Key Laboratory of Diagnosis and Treatment of Thyroid Diseases, The First Hospital of China Medical University, Shenyang, China Background: Haploinsufficiency of A20 (HA20) is a monogenic autosomal-dominant genetic autoinflammatory disease caused by loss of function mutations in the TNFAIP3 gene.

Abstract A20 is an anti-inflammatory protein that is strongly linked to human disease. Here, we find that mice expressing three distinct targeted mutations of A20’s zinc finger 7 (ZF7) ubiquitin-binding motif uniformly developed digit arthritis with features common to psoriatic arthritis, while mice expressing point mutations in A20’s OTU or ZF4 motifs did not exhibit this phenotype.