Molecule3 diseases

TNF-α

Pro-inflammatory cytokine contributing to systemic inflammation

Expression change
Elevated
Evidence level
strong
Targeted by
Infliximab, Etanercept

Expression across diseases

DiseaseRoleExpressionEvidence
Adult-Onset Still's DiseasePro-inflammatory cytokine contributing to systemic inflammationElevatedstrong
Schnitzler SyndromePro-inflammatory cytokineElevatedmoderate
TNF Receptor-Associated Periodic SyndromeLigand for TNFR1 — upstream triggerElevated during attacksestablished

Role in pathogenesis

TNF-α is elevated in sera and tissues of AOSD patients regardless of disease activity. It contributes to systemic inflammation, ferritin production, and joint damage. However, TNF-α blockade (infliximab, etanercept) has shown inconsistent results in AOSD, suggesting it is not the primary driver but rather a downstream effector.

Sources (2)

DetailsFeist E et al. (2018) Mechanisms, biomarkers and targets for adult-onset Still's diseasePubMed
DetailsKontzias A et al. (2008) Adult-onset Still's disease: pathogenesis, clinical manifestations and therapeutic advancesPubMed