Abstract
Heterozygous loss-of-function mutations in the TNFAIP3 gene cause an early-onset autoinflammatory disease named haploinsufficiency of A20 (HA20). HA20 was also identified in patients with childhood-onset autoimmune diseases and autoimmune lymphoproliferative syndrome. SLE is not only the most common systemic autoimmune disease, but also one of the most heterogeneous illnesses presenting immense challenges to diagnosis and treatment. More than 30 causative genes for monogenic SLE and lupus-like syndrome have been described, which are associated with complement component, interferon, NF-kB, self-tolerance, and other yet uncharacterized pathways.
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