ReviewFrontiers in immunology2026
Type I interferon pathway activation in connective tissue disease associated interstitial lung disease.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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5 authors.
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Abstract
Interstitial lung disease (ILD) underlies morbidity and mortality in connective tissue diseases (CTDs) such as systemic sclerosis. ILD encompasses a range of inflammatory and fibrotic pneumopathies, some of which manifest progressive characteristics. Up to 40% of ILDs are progressive, marked by radiologic progression, lung function decline, and increased symptoms. Immunosuppression is standard therapy for ILD, whereas antifibrotics like nintedanib are used in progressive fibrotic cases. Many patients deteriorate despite treatment, underscoring the need for biomarkers and targeted interventions. Type I interferon (IFN-I) signaling is implicated in CTD-ILD: interferon stimulated gene expression correlates with accelerated pulmonary decline and sustained IFN-I can precipitate ILD. In addition, IFN-I blocking agents like anifrolumab are under clinical investigation for CTD-ILD. This review examines IFN-I's role and therapeutic targeting in ILD.
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