ArticleFrontiers in immunology2025
IgG subclass-specific N-glycosylation differentiates HRCT subtypes in idiopathic inflammatory myopathies-associated ILD.
Article in Frontiers in immunology, 2025. 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
Introduction: Idiopathic inflammatory myopathies (IIMs) frequently involve interstitial lung disease (ILD), a major contributor to morbidity and mortality. However, the immunological heterogeneity across radiologic ILD subtypes remains poorly defined. This study aimed to explore whether subclass-specific IgG N-glycopeptides could distinguish high-resolution computed tomography (HRCT)-based ILD patterns in IIM patients. Methods: We analyzed plasma IgG subclass-specific N-glycopeptides in 145 IIM patients, including 98 with ILD (IIM-ILD), using intact glycopeptide mass spectrometry. Among IIM-ILD patients, 82 with available HRCT scans were classified into the three predominant subtypes: fibrotic nonspecific interstitial pneumonia (fNSIP, n=40), cellular NSIP (cNSIP, n=18), and organizing pneumonia (OP, n=24). A weighted multinomial logistic regression model was constructed using LASSO-selected glycopeptides and clinical variables. Results: Fifteen intact N-glycopeptides (IGPs) were quantified across all IIM patients. Compared to patients without ILD, IIM-ILD patients showed significant alterations in six IgG2-subclass IGPs. Crucially, distinct glycoform signatures were identified across the three HRCT subtypes: cNSIP was enriched in highly sialylated IgG2 forms; fNSIP showed elevated IgG1 and IgG3 glycoforms; and OP exhibited uniquely high IgG2-N5H4F1. These glycoforms correlated significantly with autoantibody profiles and clinical features. A multinomial logistic regression model integrating seven key IGPs and seven clinical variables achieved robust classification of the HRCT subtypes (macro-averaged AUC = 0.89). Conclusion: Subclass-specific IgG N-glycosylation profiles reflect the immunological heterogeneity underlying IIM-ILD. Integrating these glycan signatures with routine clinical data creates a strong model for distinguishing HRCT-defined endotypes, supporting their potential to improve disease classification and guide future mechanistic research in autoimmune-related ILD.
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