Observations reveal impaired thymic development and autoantibodies in a child with FOXN1 variant, suggesting new therapies.
These findings suggest that heterozygous FOXN1 variants can impair thymic development in a manner that promotes the selective emergence of neutralizing auto-Abs against type I IFNs, thereby predisposing affected individuals to severe viral infections. Monitoring these auto-Abs may support personalized therapeutic strategies for affected patients.
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Gutiérrez‐Guerrero et al. (2026) studied this question.
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