A distinct monocyte transcriptional state links systemic immune dysregulation to pulmonary impairment in long COVID.

A distinct monocyte transcriptional state links systemic immune dysregulation to pulmonary impairment in long COVID.

Publication date: Jan 14, 2026

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-_705B1-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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Concepts Keywords
Cxcl11 Covid
Driving Dysregulation
Immunological Fatigue
Monocytes Immune
Pulmonary Individuals
Lc
Long
Mo
Monocyte
Persistent
Respiratory
Severe
Showed
Systemic
Transcriptional

Semantics

Type Source Name
disease MESH long COVID
disease MESH infection
disease MESH fatigue
disease MESH dyspnea
disease MESH severe acute respiratory syndrome
disease MESH SARS CoV 2 infection
drug DRUGBANK Tretamine
disease MESH included
drug DRUGBANK Ademetionine
disease MESH AIS
drug DRUGBANK Dimercaprol
disease MESH headache
disease MESH syndrome
drug DRUGBANK Bentiromide
disease MESH IRAK4 deficiency
pathway REACTOME NOTCH1 Intracellular Domain Regulates Transcription
disease MESH Oas
pathway KEGG Platelet activation
drug DRUGBANK Oxygen
pathway REACTOME TNF signaling
pathway KEGG TNF signaling pathway
disease MESH inflammation

Original Article

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