Dysfunction of TNFAIP3/A20 Promotes Innate and Non-Infectious Hyperinflammatory Responses

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TNFAIP3, or A20, is essential for controlling inflammation and preventing excessive tissue damage.
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Mutations or haploinsufficiency of TNFAIP3 are associated with diseases characterized by inappropriate inflammation.
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Systemic inflammation from Tnfaip3 deficiency in CD11c-expressing cells occurs independently of autoreactive antibodies and lymphocytes.
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The gut microbiome does not significantly influence disease manifestations in models with impaired A20 function.
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Findings suggest that autoantibodies may be a consequence of disease rather than a causative factor in TNFAIP3-associated disorders.

Frontiers In Immunology

by Karel F. A. Van Damme, Pieter Hertens, Dorine Sichien, Katrien Van der Borght, Justine Van Moorleghem, Sofie De Prijck, Alex Klarenbeek, Els Louagie, Inés Lammens, Stijn Vanhee, Christian Vanhove, Pieter De Bleser, Steven Van Laecke, Amélie Dendooven, Hamida Hammad, Lars Vereecke, Dirk Elewaut, Geert van Loo, Bart N. Lambrecht
July 17, 2026

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