Autoimmunity最新文献

{"title":"Deciphering distinct pathogenic mechanisms of ankylosing spondylitis and systemic sclerosis via shared biomarkers ZSWIM6 and CCL3L3: Insights from an integrative bioinformatics approach.","authors":"Liangyu Huang, Jiarui Chen, Renbang Yang, Jianjun Shi, Chenxing Zhou, Tianyou Chen, Sitan Feng, Chengqian Huang, Jieping Huang, Jiang Xue, Zhongxian Zhou, Jichong Zhu, Shaofeng Wu, Xinli Zhan, Chong Liu","doi":"10.1080/08916934.2024.2445557","DOIUrl":"https://doi.org/10.1080/08916934.2024.2445557","url":null,"abstract":"<p><p>Ankylosing Spondylitis (AS) and Systemic Sclerosis (SSc) are both autoimmune diseases, albeit with distinct anatomical targets. AS primarily affects the spine and sacroiliac joints, triggering inflammation and eventual fusion of the vertebrae. SSc predominantly impacts the skin and connective tissues, leading to skin fibrosis, thickening, and potential damage to vital organs such as the lungs, heart, and kidneys. Despite their differing anatomical manifestations, inflammation serves as a pivotal factor in both conditions. Exploring the causes of the different pathogenesis of inflammation in AS and SSc could provide new insights into their treatment. We selected RNA-seq profiles of peripheral blood mononuclear cells (PBMCs) from the GEO datasets GSE73754 and GSE19617. DEGs were identified using the Limma R package with an adjusted <i>p</i>-value cutoff of < 0.05. Gene Ontology pathway analysis, SVM recursive feature elimination, and Gene Set Enrichment Analysis (GSEA) were conducted to analyze the DEGs. CIBERSORT was applied to estimate immune cell composition and its correlation with hub genes. Single-cell RNA sequencing data from peripheral blood mononuclear cells in the GSE194315 dataset were included to support differential expression analysis and biomarker identification. Additionally, single-cell RNA sequencing data from bone marrow blood samples were utilized to further validate these findings, offering complementary insights into biomarker expression across distinct sample types. A total of 762 DEGs were identified between AS patients and controls, and 441 DEGs between SSc patients and controls. Both conditions showed enrichment in the Natural killer cell mediated cytotoxicity pathway. ZSWIM6 and CCL3L3 were identified as potential biomarkers in AS and SSc, with significant diagnostic capabilities demonstrated by ROC analysis. Correlation analysis revealed associations between these biomarkers and specific immune cell types. The study utilizing ZSWIM6 and CCL3L3 as potential biomarkers provides deep insights into the distinct molecular mechanisms of SSc and AS. These findings lay the foundation for future research on targeted therapies and enhance our understanding of immune cell interactions in these autoimmune diseases.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"58 1","pages":"2445557"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142891604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"N6-methyladenosine modification of THBS1 induced by affluent WTAP promotes Graves' ophthalmopathy progression through glycolysis to affect Th17/Treg balance.","authors":"Lin-Na Li, Jie-Man Wu, Zong-Ji Zheng, Shu-Xian Li, Meng-Yi Cai, Meng-Chen Zou","doi":"10.1080/08916934.2024.2433628","DOIUrl":"https://doi.org/10.1080/08916934.2024.2433628","url":null,"abstract":"<p><p>Graves' ophthalmopathy (GO) obvious manifestation is the imbalance of Th17/Treg. N6-methyladenosine (m6A) methylation is an important regulator of Th17/Treg balance. However, few reports narrate how m6A regulators mediate the role of genes in GO progression. We explored the m6A modification of THBS1 mediated by WTAP, and the mechanism by which THBS1 regulated glycolysis and Th17/Treg balance. A total of 12 peripheral blood (4 GO samples, 4 GH samples, and 4 health samples) were collected to measure the percentage of Th17/Treg in monocytes by flow cytometry. RNA sequencing (RNA-seq) combined with MeRIP sequencing (MeRIP-seq) was used to screen differentially expressed and methylated genes. MeRIP-qPCR was performed to evaluate the m6A abundance of THBS1 after WTAP silencing. Glycolysis of CD4⁺ T cells was reflected by the lactate content and glucose uptake. The number of Th17 cells was increased in GO peripheral blood, whereas the Treg cells decreased. RNA-seq acquired 679 differentially expressed genes (308 up-regulated, and 371 down-regulated) in the CD4⁺ T cells of GO compared to healthy control. MeRIP-seq identified 3277 m6A peaks between the GO group and the healthy control group, corresponding with 2744 genes (1143 hypermethylated and 1601 hypomethylated). Combined analysis of RNA-seq and MeRIP-seq showed 81 hypermethylated and up-regulated genes. Among the six candidate genes in the PI3K-signaling pathway, THBS1 was the most significantly differentially expressed and hypermethylated. THBS1 silencing resulted in decreased lactate content and glucose uptake in CD4⁺ T cells. WTAP was significantly upregulated in CD4⁺ T cells of GO, and WTAP silencing significantly reduced m6A abundance and expression of THBS1. Upregulated and hypermethylated THBS1 mediated by WTAP promoted glycolysis of CD4⁺ T cells, affected Th17/Treg balance, and facilitated GO progression. We provided a novel potential target for GO treatment and revealed the molecular mechanism of WTAP and THBS1 in GO under the m6A perspective.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"58 1","pages":"2433628"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142845663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical correlations of serum anti-dsDNA immunoglobulin subfamilies in patients with systemic lupus erythematosus (SLE).","authors":"Jing Jing Wang, Ming Wei Lin, Dan Suan, Dimitra Beroukas, Tom P Gordon, Adrian Y S Lee","doi":"10.1080/08916934.2024.2441992","DOIUrl":"https://doi.org/10.1080/08916934.2024.2441992","url":null,"abstract":"<p><p>Systemic lupus erythematosus (SLE) is an extremely heterogenous autoimmune disorder. A key biomarker, the double stranded (ds) DNA autoantibody, provides diagnostic specificity for SLE. We analyzed anti-dsDNA by mass spectrometry (MS) to determine if ascertaining the autoantibody's heavy chain variable region (IGHV) may hold any clinical relevance. A cross-sectional study of 32 SLE patients (75% female) in a single center was performed. Serum anti-dsDNA was subjected to MS analyses. Obtained IGHV subfamilies were correlated with active clinical features of SLE, as determined by medical record reviews. We established significant associations with the presence of IGHV3-15 and active neuropsychiatric lupus (relative risk [RR] 5.71); IGHV3-21, IGHV3-23 and IGHV4-34 and leukopenia (RR 13.70, 2.14 and 10.29 respectively); and IGHV3-23 and serositis (RR 2.41) and cutaneous lesions (RR 2.82). This study provides the first evidence for the clinical benefits of deep anti-dsDNA profiling through MS, and provides an avenue for improving predictive medicine for SLE patients. Future studies with a greater number of patients, and to determine if these subfamilies have direct pathogenic properties are required.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"58 1","pages":"2441992"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142880919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and validation of susceptibility modules and hub genes in polyarticular juvenile idiopathic arthritis using WGCNA and machine learning.","authors":"Junfeng Liu, Jianhui Fan, Hongxiang Duan, Guoming Chen, Weihua Zhang, Pingxi Wang","doi":"10.1080/08916934.2024.2437239","DOIUrl":"https://doi.org/10.1080/08916934.2024.2437239","url":null,"abstract":"<p><strong>Background: </strong>Juvenile idiopathic arthritis (JIA), superseding juvenile rheumatoid arthritis (JRA), is a chronic autoimmune disease affecting children and characterized by various types of childhood arthritis. JIA manifests clinically with joint inflammation, swelling, pain, and limited mobility, potentially leading to long-term joint damage if untreated. This study aimed to identify genes associated with the progression and prognosis of JIA polyarticular to enhance clinical diagnosis and treatment.</p><p><strong>Methods: </strong>We analyzed the gene expression omnibus (GEO) dataset GSE1402 to screen for differentially expressed genes (DEGs) in peripheral blood single nucleated cells (PBMCs) of JIA polyarticular patients. Weighted gene co-expression network analysis (WGCNA) was applied to identify key gene modules, and protein-protein interaction networks (PPIs) were constructed to select hub genes. The random forest model was employed for biomarker gene screening. Functional enrichment analysis was conducted using David's online database, gene ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis to annotate and identify potential JIA pathways. Hub genes were validated using the receiver operating characteristic (ROC) curve.</p><p><strong>Results: </strong>PHLDA1, EGR3, CXCL2, and PF4V1 were identified as significantly associated with the progression and prognosis of JIA polyarticular phenotype, demonstrating high diagnostic and prognostic assessment value.</p><p><strong>Conclusion: </strong>These genes can be utilized as potential molecular biomarkers, offering valuable insights for the early diagnosis and personalized treatment of JIA polyarticular patients.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"58 1","pages":"2437239"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142852405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genome-wide analysis of abnormal splicing regulators and alternative splicing involved in immune regulation in systemic lupus erythematosus.","authors":"Bing Xu, Yuan Liu, Guangfeng Chen, Ping Jiang, Yuan Qu, Mengjie Wang, Xiliang Kao","doi":"10.1080/08916934.2024.2448463","DOIUrl":"https://doi.org/10.1080/08916934.2024.2448463","url":null,"abstract":"<p><p>Systemic lupus erythematosus (SLE) is an autoimmune disease with complex clinical manifestations and no current cure. Alternative splicing (AS) plays a key role in SLE by regulating immune-related genes, but its genome-wide regulatory mechanisms remain unclear. To investigate the involvement of abnormal splicing regulators and AS events in the immune regulation of SLE. Transcriptome data from the SLE dataset GSE162828 were analyzed for differential gene expression and AS events using bioinformatics tools. Immune infiltration analysis was conducted with CIBERSORT, and co-expression of key splicing factors (SFs) and AS events was assessed using SUVA software. A total of 5144 differentially expressed genes and 73 SFs were identified. Significant immune cell differences were observed between SLE and controls, highlighting SFs such as HNRNPDL, RBM47, TIA1, SSB, and DHX15. Eighty-three AS events were identified, with IRF9 and PTPRC emerging as key regulatory events linked to SLE. Dysregulated SFs influence AS in immune-related genes, affecting immune cell composition and SLE progression. These findings offer potential new therapeutic targets for modulating the immune microenvironment in SLE.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"58 1","pages":"2448463"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142913262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IDO1-mediated M2 macrophage polarization alleviates the progression of ankylosing spondylitis.","authors":"Kangqi Ji, Lingfei Wang, Weijie Liu, Genfeng Li, Xiaoyu Lian, Jun Fan, Chen Song, Yanpeng Jian","doi":"10.1080/08916934.2024.2441134","DOIUrl":"https://doi.org/10.1080/08916934.2024.2441134","url":null,"abstract":"<p><p>Indoleamine 2,3-dioxygenase 1 (IDO1) plays an anti-inflammatory role in autoimmune disease. However, its specific function in ankylosing spondylitis (AS) remain unclear. This study aimed to investigate the potential role of IDO1 in AS. Immunofluorescence, RT-qPCR, and western blot assays were employed to measure gene expression, while ELISA was used to quantify the release of M1 macrophage and M2 macrophage markers. CCK-8, EdU, flow cytometry, ALP staining, and Alizarin red staining (ARS) assays were conducted for functional analysis. JASPAR predicted the binding sites between PPARγ and the promoter, which were further validated by luciferase and ChIP assays. Our findings revealed that the expression of IDO1 was markedly elevated in AS patients. IDO1 overexpression promoted the proliferation of THP-1 cells and M2 macrophage polarization. Conversely, IDO1 knockdown facilitated the osteogenic differentiation of BMSCs. Furthermore, IDO1-mediated upregulation of PPARγ modulated RUNX2 transcription. PPARγ overexpression counteracted the effects of IDO1 knockdown, thereby inhibiting the osteogenic differentiation of BMSCs. In conclusion, the IDO1/PPARγ/RUNX2 signaling pathway may protect against AS by promoting M2 macrophage polarization and inhibiting osteogenic differentiation.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"58 1","pages":"2441134"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142845662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell analysis with childhood and adult systemic lupus erythematosus.","authors":"Jing Wang, Xiran Yang, Yanhua Zhang, Xuemei Jiang, Yanfang Li, Jingjing Cui, Yabin Liao","doi":"10.1080/08916934.2023.2281228","DOIUrl":"10.1080/08916934.2023.2281228","url":null,"abstract":"<p><p>Patients with systemic lupus erythematosus (SLE), a heterogeneous and chronic autoimmune disease, exhibit unique changes in the complex composition and transcriptional signatures of peripheral blood mononuclear cells (PBMCs). While the mechanism of pathogenesis for both childhood-onset SLE (cSLE) and adult-onset SLE (aSLE) remains unclear, cSLE patients are considered more unpredictable and dangerous than aSLE patients. In this study, we analysed single-cell RNA sequencing data (scRNA-seq) to profile the PBMC clusters of cSLE/aSLE patients and matched healthy donors and compared the PBMC composition and transcriptional variations between the two groups. Our analysis revealed that the PBMC composition and transcriptional variations in cSLE patients were similar to those in aSLE patients. Comparative single-cell transcriptome analysis between healthy donors and SLE patients revealed IFITM3, ISG15, IFI16 and LY6E as potential therapeutic targets for both aSLE and cSLE patients. Additionally, we observed that the percentage of pre-B cells (CD34^-) was increased in cSLE patients, while the percentage of neutrophil cells was upregulated in aSLE patients. Notably, we found decreased expression of TPM2 in cSLE patients, and similarly, TMEM150B, IQSEC2, CHN2, LRP8 and USP46 were significantly downregulated in neutrophil cells from aSLE patients. Overall, our study highlights the differences in complex PBMC composition and transcriptional profiles between cSLE and aSLE patients, providing potential biomarkers that could aid in diagnosing SLE.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"57 1","pages":"2281228"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139721427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Innovate therapeutic targets for autoimmune diseases: insights from proteome-wide mendelian randomization and Bayesian colocalization.","authors":"Qiubai Jin, Feihong Ren, Ping Song","doi":"10.1080/08916934.2024.2330392","DOIUrl":"10.1080/08916934.2024.2330392","url":null,"abstract":"<p><strong>Background: </strong>Despite growing knowledge regarding the pathogenesis of autoimmune diseases (ADs) onset, the current treatment remains unsatisfactory. This study aimed to identify innovative therapeutic targets for ADs through various analytical approaches.</p><p><strong>Research design and methods: </strong>Utilizing Mendelian randomization, Bayesian co-localization, phenotype scanning, and protein-protein interaction network, we explored potential therapeutic targets for 14 ADs and externally validated our preliminary findings.</p><p><strong>Results: </strong>This study identified 12 circulating proteins as potential therapeutic targets for six ADs. Specifically, IL12B was judged to be a risk factor for ankylosing spondylitis (<i>p</i> = 1.61E - 07). TYMP (<i>p</i> = 6.28E - 06) was identified as a protective factor for ulcerative colitis. For Crohn's disease, ERAP2 (<i>p</i> = 4.47E - 14), HP (<i>p</i> = 2.08E - 05), and RSPO3 (<i>p</i> = 6.52E - 07), were identified as facilitators, whereas FLRT3 (<i>p</i> = 3.42E - 07) had a protective effect. In rheumatoid arthritis, SWAP70 (<i>p</i> = 3.26E - 10), SIGLEC6 (<i>p</i> = 2.47E - 05), ISG15 (<i>p</i> = 3.69E - 05), and FCRL3 (<i>p</i> = 1.10E - 10) were identified as risk factors. B4GALT1 (<i>p</i> = 6.59E - 05) was associated with a lower risk of Type 1 diabetes (T1D). Interestingly, CTSH was identified as a protective factor for narcolepsy (<i>p</i> = 1.58E - 09) but a risk factor for T1D (<i>p</i> = 7.36E - 11), respectively. External validation supported the associations of eight of these proteins with three ADs.</p><p><strong>Conclusions: </strong>Our integrated study identified 12 potential therapeutic targets for ADs and provided novel insights into future drug development for ADs.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"57 1","pages":"2330392"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140183650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circ_0011058 alleviates RA pathology through the circ_0011058/miR-335-5p/CUL4B signal axis.","authors":"Xiaomei Wang, Qiuyun Xue, Qiangjun Duan, Ziyi Sun, Yajie Wu, Shuo Yang, Pengfei Xu, Huibo Cao, Faxue Liao, Xiao Wang, Chenggui Miao","doi":"10.1080/08916934.2023.2299587","DOIUrl":"10.1080/08916934.2023.2299587","url":null,"abstract":"<p><p>Our previous study found that Cullin 4B (CUL4B) inhibited rheumatoid arthritis (RA) pathology through glycogen synthase kinase-3beta (GSK3β)/canonical Wnt signalling pathway. In this work, pre-experiment and bioinformatics analysis suggested that circ_0011058 may lead to the up-regulation of CUL4B expression by inhibiting miR-335-5p. Therefore, we studied whether circ_0011058 can promote the expression of CUL4B through sponging the miR-335-5p and further promote the pathological development of RA. Bioinformatics prediction, real-time quantitative PCR (RT-qPCR), western blot (WB), double luciferase reporter gene and other relevant methods were used to study the inhibition of circ_0011058 on RA pathology and its molecular mechanism. Results showed that the expression of circ_0011058 was significantly increased in adjuvant arthritis (AA) rats and RA fibroblast-like synoviocytes (FLS). The knockout of circ_0011058 inhibited the proliferation of AA FLS and RA FLS, decreased the levels of interleukin-1 beta (IL-1β), interleukin 6 (IL-6), interleukin 8 (IL-8), and inhibited the expression of matrix metalloproteinase 3 (MMP3), fibronectin, which showed that circ_0011058 had a strong role in promoting RA pathology. Furthermore, miR-335-5p expression was reduced in AA rats and RA FLS. The highly expressed circ_0011058 directly sponged the miR-335-5p, which led to the increase of CUL4B expression and promoted the activation of the GSK3β/canonical signalling pathway. Finally, we confirmed that miR-335-5p mediated the roles of circ_0011058 in promoting RA pathological development, which showed that the circ_0011058/miR-335-5p/CUL4B signal axis was involved in RA pathology. This work was of great significance for clarifying the roles of circ_0011058 in RA pathology, and further work was needed to establish whether circ_0011058 was a potential therapeutic target or diagnostic marker for RA.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"57 1","pages":"2299587"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139519900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated bioinformatics analysis identifies autophagy-associated genes as candidate biomarkers and reveals the immune infiltration landscape in psoriasis.","authors":"Sixian Bai, Hongyu Cheng, Hao Li, Peng Bo","doi":"10.1080/08916934.2023.2259137","DOIUrl":"10.1080/08916934.2023.2259137","url":null,"abstract":"<p><p>Autophagy is implicated in the pathogenesis of psoriasis. We aimed to identify autophagy-related biomarkers in psoriasis <i>via</i> an integrated bioinformatics approach. We downloaded the gene expression profiles of GSE30999 dataset, and the \"limma\" package was applied to identify differentially expressed genes (DEGs). Then, differentially expressed autophagy-related genes (DEARGs) were identified <i>via</i> integrating autophagy-related genes with DEGs. CytoHubba plugin was used for the identification of hub genes and verified by the GSE41662 dataset. Subsequently, a series of bioinformatics analyses were employed, including protein-protein interaction network, functional enrichment, spearman correlation, receiver operating characteristic, and immune infiltration analyses. One hundred and one DEARGs were identified, and seven DEARGs were identified as hub genes and verified using the GSE41662 dataset. These validated genes had good diagnostic value in distinguishing psoriasis lesions. Immune infiltration analysis indicated that ATG5, SQSTM1, EGFR, MAPK8, MAPK3, MYC, and PIK3C3 were correlated with infiltration of immune cells. Seven DEARGs, namely ATG5, SQSTM1, EGFR, MAPK8, MAPK3, MYC, and PIK3C3, may be involved in the pathogenesis of psoriasis, which expanded the understanding of the development of psoriasis and provided important clinical significance for treatment of this disease.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"57 1","pages":"2259137"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140027304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}