2026 — Anifrolumab proposed for systemic sclerosis

One-paragraph summary

Narrative review consolidating evidence for anifrolumab (anti-IFNAR1) cross-indication expansion from approved indication (SLE, 2021) to systemic sclerosis. Type I interferons (IFN-I) are key mediators linking immune dysregulation to vascular and fibrotic damage in SSc. Reviews preclinical, translational, and emerging clinical evidence for IFN-I blockade as a novel SSc therapeutic strategy. For the project, anifrolumab cross-indication expansion is directly relevant to the HERV-mito loop framework. Type-I IFN is the loop's downstream amplifier — anti-IFNAR1 (anifrolumab) operates downstream of STING activation and is mechanism-equivalent to STING inhibition at the IFN-output step. Each new approved indication for anifrolumab validates IFN-I blockade as a cross-condition therapy class, supporting the project's chain-redundancy framing (P2.1 of the drift-detection meta-audit).

Claims as triples

• anifrolumab — modulates → type_I_IFN [evidence: anti-IFNAR1 mechanism, approved for SLE 2021; confidence: established]
• anifrolumab — bridges → fm_central_only [evidence: cross-indication therapy class relevant to HERV-mito loop downstream amplifier; confidence: bridging]
• type_I_IFN — responds_to → anifrolumab [evidence: pharmacological IFN-I blockade; confidence: established]

Triangulation notes

• Mechanism-equivalent to STING inhibition at the loop's IFN-output step. Both anifrolumab and STING inhibitors interrupt the loop downstream of HERV-W ENV / mitochondrial-DNA-release upstream drivers.
• Cross-indication expansion is the activation pattern WL-5 tracks. SSc would be anifrolumab's second indication; future expansion to Sjögren's, NPSLE, or other type-I-IFN-driven conditions would further validate the therapy class.
• Discovered via watchlist query WL-5.