ArticleFrontiers in immunology2026
Five children with haploinsufficiency of A20 caused by heterozygous mutations in the
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- The ubiquitin-editing enzyme A20 (TNFAIP3): mechanisms of activation, biological function, diseases and therapeutic targets.Molecular biomedicine · 2026Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Children with A20 haploinsufficiency, resulting from heterozygous variants in the Results: We identified five heterozygous variants in the Conclusions: HA20 is a rare monogenic early-onset auto-inflammatory disease. It can present with a variety of clinical manifestations, including Behcet disease, inflammatory bowel disease, lupus-like syndrome and periodic fever syndrome. Whole-exome sequencing should be actively considered for children who present with early-onset symptoms or features suggestive of autoimmune diseases.
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Registered trials
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