Autoimmunity最新文献_第2页

Clinical correlations of serum anti-dsDNA immunoglobulin subfamilies in patients with systemic lupus erythematosus (SLE). 系统性红斑狼疮（SLE）患者血清抗dsdna免疫球蛋白亚家族的临床相关性

IF 3.3 4区医学

Autoimmunity Pub Date : 2025-12-01 Epub Date: 2024-12-23 DOI: 10.1080/08916934.2024.2441992

Jing Jing Wang, Ming Wei Lin, Dan Suan, Dimitra Beroukas, Tom P Gordon, Adrian Y S Lee

{"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":"10.1080/08916934.2024.2441992","url":null,"abstract":"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.","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}

引用次数: 0

Risk of celiac disease, type 1 diabetes, and thyroid disease autoimmunity during the SARS-CoV-2 pandemic in South of Sweden: insights from the TRIAD study. 瑞典南部SARS-CoV-2大流行期间乳糜泻、1型糖尿病和甲状腺疾病自身免疫的风险：来自TRIAD研究的见解

IF 3.3 4区医学

Autoimmunity Pub Date : 2025-12-01 Epub Date: 2025-04-15 DOI: 10.1080/08916934.2025.2490491

Alexander Lind, Maria Naredi Scherman, Samia Hamdan, Daniel Agardh

{"title":"Risk of celiac disease, type 1 diabetes, and thyroid disease autoimmunity during the SARS-CoV-2 pandemic in South of Sweden: insights from the TRIAD study.","authors":"Alexander Lind, Maria Naredi Scherman, Samia Hamdan, Daniel Agardh","doi":"10.1080/08916934.2025.2490491","DOIUrl":"10.1080/08916934.2025.2490491","url":null,"abstract":"Recent studies have implied an increased incidence of autoimmune diseases following the SARS-CoV-2 pandemic. The objective was to determine if SARS-CoV-2 infections were associated with celiac disease (CD), type 1 diabetes (T1D), and autoimmune thyroid disease (AITD) autoantibodies in a population-based screening when the pandemic hit the South of Sweden during 2021 and 2022. Between August 2021 and June 2022 self-obtained capillary plasma samples were collected from 1088 children at 6-9 years of age and 1185 adolescents at 13-16 years of age, who were randomly invited from the general population to a screening for CD, T1D, AITD, and SARS-CoV-2 antibodies. Among children and adolescents screened for autoantibodies associated with CD, T1D and AITD, the SARS-CoV-2 infection rate was increased in tissue transglutaminase autoantibody (tTGA) positive (13/17; 76.5%) compared with tTGA negative (492/1168; 42.1%) 13-16-year-old individuals (p = 0.0057). There was no association between SARS-CoV-2 infection rate and AITD- or T1D autoantibodies. Our findings indicate a potential association between prior SARS-CoV-2 infection and screening-detected CD autoimmunity in adolescents aged 13-16 years. Further research is needed to elucidate whether ongoing CD autoimmunity increases susceptibility to infection or if SARS-CoV-2 may act as a trigger for CD autoimmunity in genetically and environmentally predisposed individuals.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"58 1","pages":"2490491"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968537","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}

引用次数: 0

YTHDF1 activates FBW7 transcription by regulating m⁶A-dependent FOXO1 to facilitate inflammatory response in ulcerative colitis-like model. 在溃疡性结肠炎样模型中，YTHDF1通过调节m6a依赖性FOXO1激活FBW7转录，促进炎症反应。

IF 3.3 4区医学

Autoimmunity Pub Date : 2025-12-01 Epub Date: 2025-05-19 DOI: 10.1080/08916934.2025.2491717

Hui Zhang, Meili Xu

{"title":"YTHDF1 activates FBW7 transcription by regulating m6A-dependent FOXO1 to facilitate inflammatory response in ulcerative colitis-like model.","authors":"Hui Zhang, Meili Xu","doi":"10.1080/08916934.2025.2491717","DOIUrl":"10.1080/08916934.2025.2491717","url":null,"abstract":"The prevalence of inflammatory bowel disease (IBD) has increased recently and lacks curative treatments. The involvement of the N6-methyladenosine (m6A) reader YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) in ulcerative colitis (UC)-like model was studied in this study. DSS was employed to induce the UC-like condition both in vitro and in vivo. TNF-α, IL-1β, IL-6, and IL-8 secretion levels were analyzed by ELISA assay. Cell vitality was determined by CCK8 assay. FOXO1 mRNA m6A level was examined using methylated RNA binding protein immunoprecipitation (Me-RIP) assay. The interactions between YTHDF1 and FOXO1 were analyzed by RIP assay. ChIP and dual luciferase reporter assays were used to explore the relationship between FOXO1 and FBW7. YTHDF1, FOXO1, and FBW7 were overexpressed in DSS-induced colon epithelial cells. YTHDF1 downregulation alleviated DSS-induced inflammation and NF-κB signal activation in colon epithelial cells. Mechanically, YTHDF1 increased FOXO1 mRNA stability in an m6A manner. YTHDF1 overexpression prevented the inhibition of FOXO1 knockdown on DSS-induced inflammation in colon epithelial cells. In addition, FOXO1 transcriptionally activated FBW7. Moreover, FOXO1 upregulation abolished the inhibitory effect of FBW7 knockdown on DSS-induced inflammation in colon epithelial cells. Animal experiments also showed that YTHDF1 deletion alleviated inflammatory response in UC-like mice. YTHDF1 promoted inflammatory response in the UC-like model by transcriptionally activating FBW7 through regulating m6A-dependent FOXO1.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"58 1","pages":"2491717"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144092023","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}

引用次数: 0

Receptor interacting protein kinase 1 activation and triggering mesangial cells necroptosis in MRL/lpr mice model of lupus nephritis. MRL/lpr小鼠狼疮性肾炎模型中受体相互作用蛋白激酶1激活引发系膜细胞坏死。

IF 3.3 4区医学

Autoimmunity Pub Date : 2025-12-01 Epub Date: 2025-06-10 DOI: 10.1080/08916934.2025.2515825

Lin Peng, Xiaodong Xu, Pengcheng Wang, Fan Yang, Xiaodong Zhu, Shuying Yang, Hongguang Xia, Zhihong Liu, Weisong Qin

{"title":"Receptor interacting protein kinase 1 activation and triggering mesangial cells necroptosis in MRL/lpr mice model of lupus nephritis.","authors":"Lin Peng, Xiaodong Xu, Pengcheng Wang, Fan Yang, Xiaodong Zhu, Shuying Yang, Hongguang Xia, Zhihong Liu, Weisong Qin","doi":"10.1080/08916934.2025.2515825","DOIUrl":"10.1080/08916934.2025.2515825","url":null,"abstract":"Lupus nephritis (LN) is the most common complication of systemic lupus erythematosus (SLE) affecting the kidneys. Receptor-interacting protein kinase 1 (RIPK1) is involved in necroptosis and inflammatory signaling. Here, we investigate the role of RIPK1 kinase activity in the pathogenesis of LN. Immunofluorescent colocalization of necroptosis with podocyte, endothelial cells, and mesangial cells was detected in the kidney of MRL/lpr mice. In vivo studies used ZJU37 (a RIPK1 inhibitor) to treat MRL/lpr mice to evaluate LN pathological alterations. In vitro, mouse mesangial cells were stimulated with DMSO, serum from MRL/lpr mice, and serum + ZJU37 to detect cell viability, cell death status, expression of necroptosis-related molecular proteins, and significant pathway alterations accompanied by necroptosis. We also conducted functional assay to validate the biological significance of the pathway changed. Firstly, the involvement of RIPK1/RIPK3/MLKL-dependent necroptosis was shown in the mesangial cells of MRL/lpr mice. Secondly, we found that ZJU37 inhibited glomerulonephritis, tubulointerstitial lesions, and vasculitis by reducing the necroptosis of mesangial cells in MRL/lpr mice. Moreover, we discovered that mesangial cells are susceptible to necroptosis when stimulated with serum from MRL/lpr animals and identified the primary altered pathways, including cytokine-cytokine receptor interaction and the PI3K-Akt signaling pathway, which could be abolished by ZJU37. Functional assay showed ZJU37 could significantly increase the migration and cell proliferation ability of mesangial cells. RIPK1 activation triggered mesangial cell necroptosis was identified in the kidneys of MRL/lpr mice and Inhibition of RIPK1 could alleviate LN by reducing the necroptosis of mesangial cells.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"58 1","pages":"2515825"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144257219","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}

引用次数: 0

Genome-wide analysis of abnormal splicing regulators and alternative splicing involved in immune regulation in systemic lupus erythematosus. 系统性红斑狼疮免疫调节中异常剪接调控因子和选择性剪接的全基因组分析。

IF 3.3 4区医学

Autoimmunity Pub Date : 2025-12-01 Epub Date: 2025-01-01 DOI: 10.1080/08916934.2024.2448463

Bing Xu, Yuan Liu, Guangfeng Chen, Ping Jiang, Yuan Qu, Mengjie Wang, Xiliang Kao

{"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":"10.1080/08916934.2024.2448463","url":null,"abstract":"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.","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}

引用次数: 0

CPN2 alleviates cryptorchidism by inhibiting the NF-κB pathway and regulating immune responses. CPN2通过抑制NF-κB通路和调节免疫应答来缓解隐睾。

IF 3.1 4区医学

Autoimmunity Pub Date : 2025-12-01 Epub Date: 2025-07-28 DOI: 10.1080/08916934.2025.2538860

Lei Wang, Lu Lu, Xia Guo, Feng Shao, Hai-Jun Ma, Yun Zhou

{"title":"CPN2 alleviates cryptorchidism by inhibiting the NF-κB pathway and regulating immune responses.","authors":"Lei Wang, Lu Lu, Xia Guo, Feng Shao, Hai-Jun Ma, Yun Zhou","doi":"10.1080/08916934.2025.2538860","DOIUrl":"10.1080/08916934.2025.2538860","url":null,"abstract":"Cryptorchidism, a common male reproductive disorder characterized by undescended testes, is associated with infertility and increased cancer risk. While its etiology remains incompletely understood, accumulating evidence suggests that immune-inflammatory responses contribute to disease progression. This study investigated the role of carboxypeptidase N subunit 2 (CPN2) in modulating immune activation and testicular pathology via the NF-κB signaling pathway. Key regulatory genes were identified through transcriptomic analysis, weighted gene co-expression network analysis (WGCNA), and machine learning approaches. A di-n-butyl phthalate (DBP)-induced rat model of cryptorchidism and CRISPR/Cas9-mediated CPN2 knockout rats were employed, alongside histological, immunohistochemical, Western blotting, and co-culture assays to explore immune activation and spermatogonial cell fate. CPN2 was identified as a pivotal factor that suppresses NF-κB activation and plasma cell infiltration. Its overexpression alleviated inflammatory cytokine production, preserved spermatogonial stem cell proliferation, and reduced apoptosis in both in vivo and in vitro models. These effects were reversed upon NF-κB activation, confirming the regulatory role of the CPN2/NF-κB axis. Our findings reveal that CPN2 mitigates cryptorchidism progression by modulating immune-inflammatory responses, highlighting it as a promising molecular target for non-surgical intervention in this condition.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"58 1","pages":"2538860"},"PeriodicalIF":3.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726967","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}

引用次数: 0

Antigen presentation-related protein APOL3 promotes anti-tumor T cell immunity and suppresses melanoma cell growth in mice. 抗原呈递相关蛋白APOL3促进小鼠抗肿瘤T细胞免疫和抑制黑色素瘤细胞生长。

IF 3.3 4区医学

Autoimmunity Pub Date : 2025-12-01 Epub Date: 2025-07-15 DOI: 10.1080/08916934.2025.2531833

Yuan Liao, Wenxia Yao, Zhaoyu Liu, Qian Peng, Xinke Zhou, Mengyuan Xie, Zesen Mai

{"title":"Antigen presentation-related protein APOL3 promotes anti-tumor T cell immunity and suppresses melanoma cell growth in mice.","authors":"Yuan Liao, Wenxia Yao, Zhaoyu Liu, Qian Peng, Xinke Zhou, Mengyuan Xie, Zesen Mai","doi":"10.1080/08916934.2025.2531833","DOIUrl":"https://doi.org/10.1080/08916934.2025.2531833","url":null,"abstract":"Melanoma is a malignant tumor with limited treatment option in advanced stages. Apolipoprotein L3 (APOL3), a protein implicated in immune regulation, has recently emerged as a potential player in tumor immunity. This research aims to explore the potential efficacy of APOL3 in melanoma. Using data from the Cancer Genome Atlas-Skin Cutaneous Melanoma (TCGA-SKCM), we identified two clusters based on 56 prognostic antigen presentation-related genes. Differential expression analysis revealed 185 genes between these two clusters, which were further narrowed down to 34 genes using univariate analysis and random survival forest dimensionality reduction. Among them, APOL3 was found to be the top-ranked gene. Afterward, the effect of APOL3 on melanoma cells was evaluated using CCK-8, EdU, and Transwell experiment. The results showed that overexpression of APOL3 decreases melanoma cell viability, clonogenicity, proliferation, migration, and invasion. Bioinformatics analysis showed the association of high/low APOL3 expression with genomic mutations characterizing melanoma. APOL3 was also found associated with T-cell infiltration levels, immune checkpoints (CD274, PDCD1, CD247, PDCD1LG2, CTLA4, TNFRSF9, TNFRSF4, and TLR9), and some immune pathways. To validate the role of APOL3 on T cell immunity, we applied B16 melanoma cells to construct the mice tumor models. The model showed that APOL3 overexpression markedly reduces melanoma tumor volume and weight while increasing interferon-γ (IFN-γ), granzyme B production, and CD3+ T cell infiltration. In conclusion, antigen presentation-related APOL3 promotes anti-tumor T-cell immunity and suppresses melanoma cell growth in-vitro and in-vivo in a murine model. These results suggested that APOL3 may serve as a promising immunotherapeutic target for the treatment of melanoma.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"58 1","pages":"2531833"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636062","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}

引用次数: 0

Animal models of autoimmunity: a relentless pursuit of accurate pre-clinical models. 自身免疫的动物模型：对准确临床前模型的不懈追求。

IF 3.3 4区医学

Autoimmunity Pub Date : 2025-12-01 Epub Date: 2025-02-05 DOI: 10.1080/08916934.2025.2461072

Laurence Morel

引用次数: 0

Alteration of telomere length and mtDNA copy number in interstitial lung disease associated with rheumatoid arthritis. 类风湿关节炎相关间质性肺疾病的端粒长度和mtDNA拷贝数改变

IF 3.3 4区医学

Autoimmunity Pub Date : 2025-12-01 Epub Date: 2025-03-04 DOI: 10.1080/08916934.2025.2473741

Giada De Benedittis, Andrea Latini, Chiara Morgante, Chiara Bonini, Eneida Cela, Barbara Kroegler, Alessandra Luciano, Marcello Chiocchi, Francesco Cavalli, Josuel Ora, Paola Rogliani, Giuseppe Novelli, Cinzia Ciccacci, Maria Sole Chimenti, Paola Conigliaro, Paola Borgiani

{"title":"Alteration of telomere length and mtDNA copy number in interstitial lung disease associated with rheumatoid arthritis.","authors":"Giada De Benedittis, Andrea Latini, Chiara Morgante, Chiara Bonini, Eneida Cela, Barbara Kroegler, Alessandra Luciano, Marcello Chiocchi, Francesco Cavalli, Josuel Ora, Paola Rogliani, Giuseppe Novelli, Cinzia Ciccacci, Maria Sole Chimenti, Paola Conigliaro, Paola Borgiani","doi":"10.1080/08916934.2025.2473741","DOIUrl":"10.1080/08916934.2025.2473741","url":null,"abstract":"Interstitial lung disease (ILD) is a common extra-articular manifestation of rheumatoid arthritis (RA). The inflammatory response in lung disease is characterized by severe oxidative stress, which enhances cellular senescence. Telomeric shortening and mitochondria dysregulation represent two hallmarks of cellular senescence. The maintenance of telomere length (TL) and mitochondrial DNA (mtDNA) copy number is preserved by many proteins, such as TERF1 and TFAM, respectively. Our aim was to evaluate the TL, the mtDNA copy number and the expression of two regulator gene factors in RA patients with (RA-ILD) and without lung involvement (RA-NILD). Eighty-five RA patients and 21 healthy subjects were enrolled. Relative TL, mtDNA copy number, and expression analysis of TERF1 and TFAM genes were measured using qPCR assay. All RA patients present a statistically significant telomere shortening; in particular, RA-ILD patients show shorter TL compared to both controls and RA-NILD. Patients with Usual Interstitial Pneumonia pattern show a more evident shortening of TL. Lastly, both RA-ILD and RA-NILD patients present a significant decrease in mtDNA copy number compared to controls. The analysis of regulatory genes showed an increase in TERF1 expression in RA patients compared to controls, also after stratification in the two subgroups, and a decrease in TFAM expression in RA patients compared to controls. These results show that the alteration of TL and mtDNA copy number in RA patients is more evident in the presence of ILD. The hypothesis is that, in these patients, oxidative stress could accelerate the shortening of telomeres and the decrease of mtDNA copy number.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"58 1","pages":"2473741"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539751","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}

引用次数: 0

IDO1-mediated M2 macrophage polarization alleviates the progression of ankylosing spondylitis. ido1介导的M2巨噬细胞极化可缓解强直性脊柱炎的进展。

IF 3.3 4区医学

Autoimmunity Pub Date : 2025-12-01 Epub Date: 2024-12-18 DOI: 10.1080/08916934.2024.2441134

Kangqi Ji, Lingfei Wang, Weijie Liu, Genfeng Li, Xiaoyu Lian, Jun Fan, Chen Song, Yanpeng Jian

{"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":"10.1080/08916934.2024.2441134","url":null,"abstract":"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.","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}

引用次数: 0