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pmid:38917217

Exploring the pathogenesis and immunological profiles of psoriasis complicated with MASLD.

Shuhui Tan · Mingyue Liu · Fei Feng · Ruicheng Li · Rui Tian · Zhenhua Nie

PloS one · 2024 doi:10.1371/journal.pone.0305217

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complete

Experiment

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Data

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Analysis

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pmid:38917217
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title
Exploring the pathogenesis and immunological profiles of psoriasis complicated with MASLD.
doi
10.1371/journal.pone.0305217
pmid
38917217
authors array · 6 items
[0]
Shuhui Tan
[1]
Mingyue Liu
[2]
Fei Feng
[3]
Ruicheng Li
[4]
Rui Tian
[5]
Zhenhua Nie
journal
PloS one
year
2024
abstract
BACKGROUND: Both psoriasis and metabolic dysfunction-associated steatotic liver disease (MASLD) are immune-mediated chronic inflammatory diseases. Psoriasis manifests itself mainly as skin damage, while MASLD mainly involves the liver promoting liver fibrosis, which has a significant impact on patient health and quality of life. Some clinical studies have shown that there are mutually reinforcing mechanisms between these two diseases, but they are not clearly defined, and this paper aims to further explore their common pathogenesis. METHODS: Gene expression profiling datasets (GSE30999, GSE48452) and single cell datasets (GSE151177, GSE186328) for psoriasis and MASLD were downloaded from the Gene Expression Omnibus (GEO) database. Common differential gene sets were obtained by gene differential analysis, and then functional enrichment of differential genes was performed to find associated transcription factors and PPI protein network analysis. Single-cell datasets were validated for gene expression and explored for cellular communication, gene set differential analysis and immune infiltration analysis. RESULTS: We identified seven common differential genes, all of which were upregulated.The IL-17 pathway, tumor necrosis factor (TNF-α) pathway were shown in strong association with both diseases, and five transcription factors regulating the differential genes were predicted. Two key genes (MMP9, CXCL10) and three key transcription factors (TF) (IRF1, STAT1, NFKB1) were obtained by PPI protein network analysis. Single cell dataset verified the expression of key genes, and combined with gene set differential analysis, immune infiltration revealed that CD4+ T cells, NK cells and macrophages were heavily infiltrated in both diseases. IL-17, IL-1 and cGAS-STING pathways were highly expressed in both diseases, and both diseases share a similar immune microenvironment. CONCLUSIONS: Our study reveals the common pathogenesis of psoriasis and MASLD from gene expression to immune cell similarities and differences, identifies key genes and regulatory pathways common to both, and elucidates the similarities in the immune microenvironment of both diseases, providing new ideas for subsequent studies on targeted therapy.
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Differential gene analysis was performed on each of the two datasets using the ’limma’ package to obtain differentially expressed genes (DEGs) in disease versus normal subjects, with statistically defined criteria for differential genes being log2FC>1 and adj. P.val<0.05.
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Differential gene analysis was performed on each of the two datasets using the ’limma’ package to obtain differentially expressed genes (DEGs) in disease versus normal subjects, with statistically defined criteria for differential genes being log2FC>1 and adj. P.val<0.05.
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The datasets (GSE30999, GSE48452, GSE151177, GSE186328) analyzed during this study are publicly available in the Gene Expression Omnibus database (http://www.ncbi.nlm.nih.gov/geo). The original contributions presented in the study are included in the article/supplementary material. Further inquiries can be directed to the authors.
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sections[22] "Data Availability" paragraph 2
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The datasets (GSE30999, GSE48452, GSE151177, GSE186328) analyzed during this study are publicly available in the Gene Expression Omnibus database (http://www.ncbi.nlm.nih.gov/geo). The original contributions presented in the study are included in the article/supplementary material. Further inquiries can be directed to the authors.
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We identified seven common differential genes, all of which were upregulated.
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Seven common differential genes were identified, and all were upregulated.
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Differential gene analysis was performed on each of the two datasets using the ’limma’ package to obtain differentially expressed genes (DEGs) in disease versus normal subjects, with statistically defined criteria for differential genes being log2FC>1 and adj. P.val<0.05.
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Automated Assays Laravel application and simulated adapters
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capability object · 4 fields
tier
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data object · 6 fields
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statements array · 1 item
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The datasets (GSE30999, GSE48452, GSE151177, GSE186328) analyzed during this study are publicly available in the Gene Expression Omnibus database (http://www.ncbi.nlm.nih.gov/geo). The original contributions presented in the study are included in the article/supplementary material. Further inquiries can be directed to the authors.
basis
The paper names GSE30999, GSE48452, GSE151177, GSE186328 in Gene Expression Omnibus (GEO) database and the accession resolves in the repository. No dataset was downloaded and no licence was read.
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minimax
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independence
single_reader
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GEO GSE151177
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PMID 38917217 full text
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GEO GSE151177
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agent:corpus-assay-engine
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Differential gene analysis was performed on each of the two datasets using the ’limma’ package to obtain differentially expressed genes (DEGs) in disease versus normal subjects, with statistically defined criteria for differential genes being log2FC>1 and adj. P.val<0.05.
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{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:38917217", "kind": "science-record", "revision": 4, "content_hash": "sha256:bce84db4b9f973fd478eb22d4eb3982902c2def029ba9e8392804019cef5d685", "created_at": "2026-11-01T20:28:59Z", "updated_at": "2026-11-01T22:54:34Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "Exploring the pathogenesis and immunological profiles of psoriasis complicated with MASLD.", "doi": "10.1371/journal.pone.0305217", "pmid": "38917217", "authors": ["Shuhui Tan", "Mingyue Liu", "Fei Feng", "Ruicheng Li", "Rui Tian", "Zhenhua Nie"], "journal": "PloS one", "year": 2024, "abstract": "BACKGROUND: Both psoriasis and metabolic dysfunction-associated steatotic liver disease (MASLD) are immune-mediated chronic inflammatory diseases. Psoriasis manifests itself mainly as skin damage, while MASLD mainly involves the liver promoting liver fibrosis, which has a significant impact on patient health and quality of life. Some clinical studies have shown that there are mutually reinforcing mechanisms between these two diseases, but they are not clearly defined, and this paper aims to further explore their common pathogenesis.\nMETHODS: Gene expression profiling datasets (GSE30999, GSE48452) and single cell datasets (GSE151177, GSE186328) for psoriasis and MASLD were downloaded from the Gene Expression Omnibus (GEO) database. Common differential gene sets were obtained by gene differential analysis, and then functional enrichment of differential genes was performed to find associated transcription factors and PPI protein network analysis. Single-cell datasets were validated for gene expression and explored for cellular communication, gene set differential analysis and immune infiltration analysis.\nRESULTS: We identified seven common differential genes, all of which were upregulated.The IL-17 pathway, tumor necrosis factor (TNF-α) pathway were shown in strong association with both diseases, and five transcription factors regulating the differential genes were predicted. Two key genes (MMP9, CXCL10) and three key transcription factors (TF) (IRF1, STAT1, NFKB1) were obtained by PPI protein network analysis. Single cell dataset verified the expression of key genes, and combined with gene set differential analysis, immune infiltration revealed that CD4+ T cells, NK cells and macrophages were heavily infiltrated in both diseases. IL-17, IL-1 and cGAS-STING pathways were highly expressed in both diseases, and both diseases share a similar immune microenvironment.\nCONCLUSIONS: Our study reveals the common pathogenesis of psoriasis and MASLD from gene expression to immune cell similarities and differences, identifies key genes and regulatory pathways common to both, and elucidates the similarities in the immune microenvironment of both diseases, providing new ideas for subsequent studies on targeted therapy.", "claims": [{"id": "claim-method", "statement": "Differential gene analysis was performed on each of the two datasets using the ’limma’ package to obtain differentially expressed genes (DEGs) in disease versus normal subjects, with statistically defined criteria for differential genes being log2FC>1 and adj. P.val<0.05.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:38917217", "locator": "sections[4] \"2.2. Identification of DEGs\" paragraph 2", "quote": "Differential gene analysis was performed on each of the two datasets using the ’limma’ package to obtain differentially expressed genes (DEGs) in disease versus normal subjects, with statistically defined criteria for differential genes being log2FC>1 and adj. P.val<0.05."}], "state": "complete"}, {"id": "claim-data-access", "statement": "The datasets (GSE30999, GSE48452, GSE151177, GSE186328) analyzed during this study are publicly available in the Gene Expression Omnibus database (http://www.ncbi.nlm.nih.gov/geo). The original contributions presented in the study are included in the article/supplementary material. Further inquiries can be directed to the authors.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:38917217", "locator": "sections[22] \"Data Availability\" paragraph 2", "quote": "The datasets (GSE30999, GSE48452, GSE151177, GSE186328) analyzed during this study are publicly available in the Gene Expression Omnibus database (http://www.ncbi.nlm.nih.gov/geo). The original contributions presented in the study are included in the article/supplementary material. Further inquiries can be directed to the authors."}], "state": "complete"}, {"id": "claim-target-result", "statement": "Seven common differential genes were identified, and all were upregulated.", "kind": "qualitative", "target": null, "evidence": [{"asset": "source:pmid:38917217", "locator": "sections[0] \"Abstract\" paragraph 3", "quote": "We identified seven common differential genes, all of which were upregulated."}], "state": "complete"}], "gaps": []}, "experiment": {"state": "complete", "objective": "Seven common differential genes were identified, and all were upregulated.", "steps": [{"id": "read_published_estimate", "order": 1, "name": "Read the published estimate from the source", "kind": "other", "state": "complete", "blocked_on": null, "description": "The claim, method and evidence span published with the source article.", "duration_hours": null, "parameters": {}, "inputs": ["source:pmid:38917217"], "outputs": ["the published estimate and its evidence"], "instruments": [], "reagents": []}, {"id": "obtain_source_data", "order": 2, "name": "Obtain the source data from the named repository", "kind": "data-preparation", "state": "complete", "blocked_on": null, "description": "The GEO series accession resolves and its sample accessions are listed. This lane did not download the dataset or read its licence.", "duration_hours": null, "parameters": {}, "inputs": ["data:geo:GSE151177"], "outputs": ["the source data with its repository provenance"], "instruments": [], "reagents": []}, {"id": "run_analysis", "order": 3, "name": "Run the published analysis", "kind": "analysis", "state": "complete", "blocked_on": null, "description": "Apply the paper's statistical method to the resolved series and compare the result with the published target.", "duration_hours": null, "parameters": {}, "inputs": ["data:geo:GSE151177"], "outputs": ["the replicated result and its comparison"], "instruments": [], "reagents": []}], "materials": [], "instruments": [], "reagents": [], "conditions": {}, "gaps": []}, "data": {"state": "partial", "assets": [{"id": "source:pmid:38917217", "role": "manuscript", "format": "xml", "media_type": "application/xml", "uri": "https://doi.org/10.1371/journal.pone.0305217", "sha256": "sha256:173ec3247d7f3503d80ee2ea7b69603f36da8cab95340b07c53c7d915d6615e9", "bytes": 41095, "access": "open", "state": "resolved", "reader": null, "reader_status": "reader_required", "identifier": "10.1371/journal.pone.0305217", "version": null, "note": "Full article fetched from PMC; the checksum covers the rendered section body, not the original XML bytes.", "structure": {"pmcid": "PMC11198785", "source": "europe_pmc_fulltext", "coverage": "whole_body", "text_hash_scope": "rendered_section_body"}}, {"id": "data:geo:GSE151177", "role": "raw", "format": "geo-series", "media_type": "application/vnd.ncbi.geo-series+json", "uri": "https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE151177", "sha256": null, "bytes": null, "access": "open", "state": "resolved", "reader": null, "reader_status": "reader_required", "identifier": "GSE151177", "version": null, "note": "The datasets (GSE30999, GSE48452, GSE151177, GSE186328) analyzed during this study are publicly available in the Gene Expression Omnibus database (http://www.ncbi.nlm.nih.gov/geo). The original contributions presented in the study are included in the article/supplementary material. Further inquiries can be directed to the authors.", "structure": {"repository": "GEO", "access_route": "GEO accession URL", "access_statement_verbatim": "The datasets (GSE30999, GSE48452, GSE151177, GSE186328) analyzed during this study are publicly available in the Gene Expression Omnibus database (http://www.ncbi.nlm.nih.gov/geo). The original contributions presented in the study are included in the article/supplementary material. 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Further inquiries can be directed to the authors.", "access_statement_kind": "data_availability_statement", "sample_accessions": ["GSM5643817", "GSM5643818", "GSM5643819", "GSM5643820", "GSM5643821", "GSM5643822"], "sample_count": 6, "group_sizes": null, "group_sizes_basis": null, "platform": "24676", "taxon": "Homo sapiens", "title": "Activation of GPR3-b-Arrestin2-PKM2 by DPI enhanced glycolysis in kupffer cells [single-cell RNA-seq]", "resolution_checked_at": "2026-11-01T20:16:08Z", "resolution_check": "identifier_resolution_only_no_download_no_licence_read", "downloaded": false, "licence_read": false}}, {"id": "data:geo:GSE30999", "role": "raw", "format": "geo-series", "media_type": "application/vnd.ncbi.geo-series+json", "uri": "https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE30999", "sha256": null, "bytes": null, "access": "open", "state": "resolved", "reader": null, "reader_status": "reader_required", "identifier": "GSE30999", "version": null, "note": "The datasets (GSE30999, GSE48452, GSE151177, GSE186328) analyzed during this study are publicly available in the Gene Expression Omnibus database (http://www.ncbi.nlm.nih.gov/geo). 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