ArticleTuberculosis and respiratory diseases2026
Single-Cell Analysis Identifies Factors Associated with Rheumatoid Arthritis-Related Interstitial Lung Disease in Comparison with Idiopathic Pulmonary Fibrosis.
Article in Tuberculosis and respiratory diseases, 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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Abstract
backgroundInterstitial lung disease (ILD) is a common but serious extra-articular manifestation of rheumatoid arthritis (RA). RA-associated ILD (RA-ILD), which often presents with the usual interstitial pneumonia pattern, can resemble idiopathic pulmonary fibrosis (IPF), though the treatment and progression of these two conditions differ. However, the immunologic and molecular mechanisms associated with RA-ILD and IPF development have not been well elucidated at the single-cell level.
methodsTo investigate the underlying mechanisms associated with RA-ILD and IPF development, we performed single-cell RNA sequencing (scRNA-seq) of peripheral blood mononuclear cells (PBMCs) from five RA-ILD patients and five patients with IPF with a matched age and sex distribution.
resultsA high-quality scRNA-seq dataset comprising 31,416 peripheral immune cells was generated. Overall immune composition was similar between groups; however, a significant elevation of natural killer (NK) cells was seen among the RA-ILD PBMCs, with increased expression of cytotoxic and inflammation-related genes (GZMB, GZMH, PRF1) as well as interferon‑related genes (STAT1, STAT3, IRF9, IFNG). Myeloid subsets displayed distinct transcriptional programs in IPF and RA-ILD: IPF CD16+ monocytes were enriched for transforming growth factor beta (TGF‑β)-driven fibrotic signaling, whereas RA-ILD monocytes exhibited type I/II interferon pathway activation. Fibrosis‑related genes (TGFB1, SMAD3, SMAD7, TGIF1) were specifically upregulated in IPF.
conclusionRA‑ILD and IPF share similar peripheral immune cell compositions, but exhibit distinct transcriptional activation patterns. RA‑ILD is characterized by increased NK‑cell-driven cytotoxic and interferon‑related responses, along with interferon‑activated monocytes. In contrast, IPF shows a TGF‑β-dominant fibrotic program, with transcriptional activation of CD16+ monocytes and upregulation of fibrosis‑related genes.
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