Authors
Benjamin J Schmiedel, Cristian Gonzalez-Colin, Vicente Fajardo-Rosas, Job Rocha, Hayley Simon, Johannes Ottensmeier, Ignacio E Ramírez-Bernabé, April Cano, Angel De la Cruz Castillo, Elizabeth Márquez-Gómez, Brendan Ha, Jason A Greenbaum, Lindsey Chudley, Judith Cave, Aiman Alzetani, Edwin Woo, Michael Shackcloth, Serena J Chee, Vivek Chandra, Mitchell Kronenberg, Bjoern Peters, Christian H Ottensmeier, Anusha-Preethi Ganesan, Pandurangan Vijayanand
Published in
Nature immunology. Aug 03, 2026. Epub Aug 03, 2026.
Abstract
Common genetic variants are associated with risk of lung and autoimmune diseases. However, we have a limited understanding of the pathological effects of these disease variants, specifically in tissue-resident immune cells at the frontier of infection and disease in the lung. To address this, we performed single-cell expression quantitative trait locus (eQTL) analysis across 29 distinct immune cell subsets isolated from lung tissue. Colocalization analysis of lung immune cell eQTLs with genome-wide association study (GWAS) signals from lung diseases, and infectious and autoimmune diseases, implicate disease-associated variants and their target genes functioning in a single or restricted group of cell types. Several genes, including ZFP57, showed significant colocalization between lung immune cell eQTLs and GWAS signals from multiple systemic and organ-restricted autoimmune diseases, highlighting shared genetic mechanisms underlying the risk of disease. Overall, our study shows that disease-associated variants from a wide range of autoimmune diseases impact gene expression in tissue-resident immune cell types ( https://lung.dice-database.org ).
PMID:
42547572
Bibliographic data and abstract were imported from PubMed on 04 Aug 2026.
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