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Changes in macrophage transcriptome associate with systemic sclerosis and mediate GSDMA contribution to disease risk
Open accessAbstract
Objectives Several common and rare risk variants have been reported for systemic sclerosis (SSc), but the effector cell(s) mediating the function of these genetic variants remains to be elucidated. While innate immune cells have been proposed as the critical targets to interfere with the disease process underlying SSc, no studies have comprehensively established their effector role. Here we investigated the contribution of monocyte-derived macrophages (MDMs) in mediating genetic susceptibility to SSc. Methods We carried out RNA sequencing and genome-wide genotyping in MDMs from 57 patients with SSc and 15 controls. Our differential expression and expression quantitative trait locus (eQTL) analysis in SSc was further integrated with epigenetic, expression and eQTL data from skin, monocytes, neutrophils and lymphocytes. Results We identified 602 genes upregulated and downregulated in SSc macrophages that were significantly enriched for genes previously implicated in SSc susceptibility (P=5×10−4), and 270 cis-regulated genes in MDMs. Among these, GSDMA was reported to carry an SSc risk variant (rs3894194) regulating expression of neighbouring genes in blood. We show that GSDMA is upregulated in SSc MDMs (P=8.4×10−4) but not in the skin, and is a significant eQTL in SSc macrophages and lipopolysaccharide/interferon gamma (IFNγ)-stimulated monocytes. Furthermore, we identify an SSc macrophage transcriptome signature characterised by upregulation of glycolysis, hypoxia and mTOR signalling and a downregulation of IFNγ response pathways. Conclusions Our data further establish the link between macrophages and SSc, and suggest that the contribution of the rs3894194 risk variant to SSc susceptibility can be mediated by GSDMA expression in macrophages.
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Patients with systemic sclerosis have higher expression of GRB10 in monocytes.
“GRB10 has been associated with a subtype of systemic sclerosis (lcSSc); patients with systemic sclerosis have higher expression of GRB10 in monocytes67,68.”
From Quantifying the contribution of Neanderthal introgression to the heritability of complex traits (2021) · cites this paper as [68]
The Results (Differential expression analysis of SSc and control MDMs; page unavailable) identify GRB10 among genes upregulated in patients with systemic sclerosis. However, the cells studied were monocyte-derived macrophages, not monocytes, so the cited paper does not establish higher GRB10 expression in monocytes. (LLM, conf=0.87)
Experimental — accuracy not yet measuredGRB10 has been associated with a subtype of systemic sclerosis (lcSSc).
“GRB10 has been associated with a subtype of systemic sclerosis (lcSSc); patients with systemic sclerosis have higher expression of GRB10 in monocytes67,68.”
From Quantifying the contribution of Neanderthal introgression to the heritability of complex traits (2021) · cites this paper as [68]
The Results (Differential expression analysis of SSc and control MDMs; page unavailable) state that GRB10 had previously been associated with SSc subphenotypes by GWAS. The passage does not identify the associated subtype as limited cutaneous SSc (lcSSc), so it supports the general association but not that specificity. (LLM, conf=0.84)
Experimental — accuracy not yet measuredTo get realistic estimates for effect sizes (fold changes), data sets from FACS sorted bulk RNA-seq studies were taken53,54.
“To get realistic estimates for effect sizes (fold changes), data sets from FACS sorted bulk RNA-seq studies were taken53,54.”
From scPower accelerates and optimizes the design of multi-sample single cell transcriptomic studies (2021) · cites this paper as [54]
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Metadata
- Authors
- Moreno-Moral, A., Bagnati, M., Koturan, S., Ko, J.-H., Fonseca, C., Harmston, N., Game, L., Martin, J., Ong, V., Abraham, D. J., Denton, C. P., Behmoaras, J., & Petretto, E.
- Affiliations
- Hammersmith Hospital (GB)
- The Royal Free Hospital (GB)
- Duke-NUS Medical School (SG)
- Consejo Superior de Investigaciones Científicas (ES)
- Corresponding author
- Behmoaras, Jacques
- ORCID
- Venue
- Annals of the Rheumatic Diseases
- Publisher
- Elsevier BV
- Published
- 2018-04
- Volume
- 77
- Issue
- 4
- Pages
- 596-601
- ISSN
- 0003-4967 (ISSN-L)
- PMC
- PMC5890626
- OpenAlex
- W2783530444
- Semantic Scholar
- 6a427ebe286ca57bf5e2e2d1122061fdcfe9130f
- Cited by
- 78
- References
- 37
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 11 · 2023: 8 · 2022: 14 · 2021: 15 · 2020: 10 · 2019: 4 · 2018: 6
- FWCI
- 6.66
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Annals of the Rheumatic Diseases (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion, cc-by)
- National University of Singapore (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- ORCA Online Research @Cardiff (Cardiff University) (submittedVersion)
- HighWire Press Open Archive (submittedVersion)
- Spiral (Imperial College London) (submittedVersion, other-oa)
- Funders
- Scleroderma & Raynaud’s UK and The Royal Free Charity
- Arthritis Research UK
- Spanish National Program for Knowledge Generation, Subprograma Estatal de Generación de Conocimiento
- Duke-NUS Medical School
- National Medical Research Council
- Medical Research Council
- Topics
- Health Sciences › Medicine › Rheumatology › Systemic Sclerosis and Related Diseases
- Health Sciences › Medicine › Rheumatology › Dupuytren's Contracture and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- systemic sclerosis, macrophages, monocyte-derived macrophages, GSDMA, genetic susceptibility, expression quantitative trait loci, macrophage transcriptome, innate immunity, interferon-gamma response, glycolysis, hypoxia, mTOR signaling
- MeSH terms
- Gasdermins, Adolescent, Adult, Child, Child, Preschool, Female, Humans, Macrophages, Male, Neoplasm Proteins, Risk Factors, Scleroderma, Systemic, Skin, Signal Transduction, Case-Control Studies, Genetic Predisposition to Disease, Quantitative Trait Loci, Young Adult, Transcriptome, Genotyping Techniques
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