ArticleNature immunology2026
A distinct monocyte transcriptional state links systemic immune dysregulation to pulmonary impairment in long COVID.
Article in Nature immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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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Who cites it
5 citing papers in PubMed.
- Distinct Regulatory DNA Methylation Signatures Across Multiple Sclerosis, Neuromyelitis Optica, and Neurological Post-Acute Sequelae of COVID-19.Journal of clinical medicine · 2026Article
- Reframing ME/CFS: toward a unified mechanistic model of chronic post-infectious diseases.Journal of translational medicine · 2026Review
- Comprehensive Immunophenotyping of Monocytes and Dendritic Cells Suggests Distinct Pathophysiology in Chronic Fatigue Syndrome and Long COVID.International journal of molecular sciences · 2026Article
- CROI 2026: Acute and Postacute COVID-19.Topics in antiviral medicine · 2026Article
- Immunologically distinct long COVID after mild acute disease.Nature immunology · 2026Article
Corrections and comments
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Authors and funding
26 authors.
Funding
Abstract
The mechanisms driving immune dysregulation in long COVID disease remain elusive. Here we integrated single-cell multiome data, immunological profiling and functional assays to investigate immune alterations across multiple cohorts. A transcriptional state in circulating monocytes (LC-Mo) was enriched in individuals with mild-moderate acute infection and accompanied by persistent elevations of plasma CCL2, CXCL11 and TNF. LC-Mo showed TGFβ and WNT-β-catenin signaling and correlated with fatigue severity. Protein markers of LC-Mo were increased in individuals with pronounced fatigue or dyspnea, and those with severe respiratory symptoms showed higher LC-Mo expression. Epigenetically, LC-Mo exhibited AP-1- and NF-κB1-driven profibrotic programs. LC-Mo-like macrophages in bronchoalveolar lavage samples from individuals with severe respiratory symptoms displayed a profibrotic profile, and individuals with a high LC-Mo transcriptional state showed impaired interferon responses after stimulation. Collectively, our findings define a pathogenic monocyte transcriptional state linking systemic immune dysfunction to persistent long COVID disease, providing mechanistic insights and potential therapeutic targets.
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