Immunological Investigations最新文献

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Up Regulation of ZNF76 rs10947540 and SCUBE3 rs1888822 Single Nucleotide Polymorphisms as a Genetic Risk Factor in Egyptian Patients with Rheumatoid Arthritis. ZNF76 rs10947540和SCUBE3 rs1888822单核苷酸多态性上调在埃及类风湿关节炎患者中的遗传风险因素
IF 2.9 4区 医学
Immunological Investigations Pub Date : 2025-01-01 Epub Date: 2024-12-19 DOI: 10.1080/08820139.2024.2418569
Eman Abd Allah Fouda, Alshimaa Mohamed Elmalawany, Eman Masoud Abd El Gayed, Salah Mohamed El-Kousy, Heba Saber Mohamed, Ahmed B Zaid, Mohamed Farag Ali Assar
{"title":"Up Regulation of <i>ZNF76</i> rs10947540 and <i>SCUBE3</i> rs1888822 Single Nucleotide Polymorphisms as a Genetic Risk Factor in Egyptian Patients with Rheumatoid Arthritis.","authors":"Eman Abd Allah Fouda, Alshimaa Mohamed Elmalawany, Eman Masoud Abd El Gayed, Salah Mohamed El-Kousy, Heba Saber Mohamed, Ahmed B Zaid, Mohamed Farag Ali Assar","doi":"10.1080/08820139.2024.2418569","DOIUrl":"10.1080/08820139.2024.2418569","url":null,"abstract":"<p><strong>Introduction: </strong>The protein <i>SCUBE3</i> has been observed to exhibit an association with various autoimmune conditions, including psoriasis and rheumatoid arthritis. Genetic experiments have revealed that changes in Zinc finger protein-coding sequences correlate with an increased vulnerability to developing autoimmune diseases, so we aimed to study investigates the involvement of <i>ZNF76</i> rs10947540 and <i>SCUBE3</i> rs1888822 gene expression in individuals diagnosed with Rheumatoid Arthritis.</p><p><strong>Methods: </strong>In a case-control study conducted from January 2022 to March 2023, 80 adults with RA from Menoufia University Hospital were compared with 80 age- and gender-matched healthy controls. Single nucleotide polymorphisms (SNPs) <i>ZNF76</i> rs10947540 and <i>SCUBE3</i> rs1888822 were analysed using real-time polymerase chain reaction (PCR).</p><p><strong>Results: </strong>ZNF76 rs10947540 demonstrated a 7.125-fold increased risk for RA in CC genotype individuals and a 2.958-fold risk associated with the C allele. Those with the TC genotype had a 2.523-fold increased risk. Similarly, <i>SCUBE3</i> rs1888822 showed a 6.364-fold risk for RA in TT genotype individuals and a 3.065-fold risk for T allele carriers. GT genotype individuals had a 2.765-fold risk.</p><p><strong>Discussion: </strong>Our study suggests that <i>ZNF76</i> rs10947540 and <i>SCUBE3</i> rs1888822 polymorphisms may be risk factors for RA in Egyptian patients. Understanding the genetic variations associated with higher risk underscores the role of genetics in RA progression.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"46-67"},"PeriodicalIF":2.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853995","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
Tectochrysin Alleviates Periodontitis by Modulating M2/M1 Macrophage Ratio and Oxidative Stress Via Nuclear Factor Kappa B/Heme Oxygenase-1/Nuclear Factor Erythroid 2-Related Factor 2 Pathway. 通过核因子 Kappa B/Heme 氧化酶-1/核因子红细胞 2 相关因子 2 途径调节 M2/M1 巨噬细胞比例和氧化应激,从而缓解牙周炎。
IF 2.9 4区 医学
Immunological Investigations Pub Date : 2025-01-01 Epub Date: 2024-10-29 DOI: 10.1080/08820139.2024.2418938
Ye Yin, Yanming Weng, Zeyu Ma, Li Li
{"title":"Tectochrysin Alleviates Periodontitis by Modulating M2/M1 Macrophage Ratio and Oxidative Stress Via Nuclear Factor Kappa B/Heme Oxygenase-1/Nuclear Factor Erythroid 2-Related Factor 2 Pathway.","authors":"Ye Yin, Yanming Weng, Zeyu Ma, Li Li","doi":"10.1080/08820139.2024.2418938","DOIUrl":"10.1080/08820139.2024.2418938","url":null,"abstract":"<p><strong>Background: </strong>Tectochrysin suppresses several diseases. In this study, we aimed to explore the effects of tectochrysin ona rat model of periodontitis PDS).</p><p><strong>Methods: </strong>Male Sprague-Dawley (SD) rats were subjected to ligature to induce periodontitis. Bone parameters were analyzed using micro-computed tomography and periodontal tissues were evaluated using Masson's, hematoxylin and eosin, and tartrate-resistant acid phosphatase staining. The expression of HO-1, Nrf2, CD206, Arg-1, and iNOS was evaluated using immunohistochemistry. Malondialdehyde (MDA), reduced glutathione (GSH), and superoxide dismutase (SOD) levels and IL-1β, IL-6, and tumor necrosis factor (TNF)-α,and NF-κB and Nrf2/HO-1 were analyzed.</p><p><strong>Results: </strong>Tectochrysin reduced alveolar bone loss, promoted new bone formation, and inhibited osteoclast formation in periodontitis rats. It decreased the number of inflammatory cells and the levels of IL-1β, IL-6, and TNF-α, indicating a reduction in inflammation. Tectochrysin restored the Arg-1/iNOS ratio, indicating M2 macrophage polarization, and inhibited the NF-kB pathway. Tectochrysin restored GSH and SOD levels, inhibited MDA content, and activated the HO-1/Nrf2 pathway.</p><p><strong>Conclusion: </strong>Tectochrysin alleviates PDS in rats by modulating the M2/M1 macrophage ratio via the NF-kB pathway and suppressing oxidative stress via the HO-1/Nrf2 pathway.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"97-111"},"PeriodicalIF":2.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142521816","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
Integration of Gut Mycobiota and Oxidative Stress to Decipher the Roles of C-Type Lectin Receptors in Inflammatory Bowel Diseases. 整合肠道霉菌生物群和氧化应激,破解 C 型直链蛋白受体在炎症性肠病中的作用。
IF 2.9 4区 医学
Immunological Investigations Pub Date : 2024-11-01 Epub Date: 2024-08-08 DOI: 10.1080/08820139.2024.2388164
Liu Yang, Min Hu, Jing Shao
{"title":"Integration of Gut Mycobiota and Oxidative Stress to Decipher the Roles of C-Type Lectin Receptors in Inflammatory Bowel Diseases.","authors":"Liu Yang, Min Hu, Jing Shao","doi":"10.1080/08820139.2024.2388164","DOIUrl":"10.1080/08820139.2024.2388164","url":null,"abstract":"<p><strong>Background: </strong>Ulcerative colitis (UC) and Crohn's disease (CD) are two subtypes of inflammatory bowel disease (IBD) with rapidly increased incidence worldwide. Although multiple factors contribute to the occurrence and progression of IBD, the role of intestinal fungal species (gut mycobiota) in regulating the severity of these conditions has been increasingly recognized. C-type lectin receptors (CLRs) on hematopoietic cells, including Dectin-1, Dectin-2, Dectin-3, Mincle and DC-SIGN, are a group of pattern recognition receptors (PRRs) that primarily recognize fungi and mediate defense responses, such as oxidative stress. Recent studies have demonstrated the indispensable role of CLRs in protecting the colon from intestinal inflammation and mucosal damage.</p><p><strong>Methods and results: </strong>This review provides a comprehensive overview of the role of CLRs in the pathogenesis of IBD. Given the significant impact of mycobiota and oxidative stress in IBD, this review also discusses recent advancements in understanding how these factors exacerbate or ameliorate IBD. Furthermore, the latest developments in CLR-guided IBD therapy are examined to highlight the modulation of CLRs in fungal recognition and oxidative burst during the IBD process.</p><p><strong>Conclusion: </strong>This review emphasizes the importance of CLRs in IBD, offering new perspectives on the etiology and therapeutic approaches for this disease.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1177-1204"},"PeriodicalIF":2.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141906496","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
Statement of Retraction: Prophylactic Effect of BIO-1211 Small-Molecule Antagonist of VLA-4 in the EAE Mouse Model of Multiple Sclerosis. 撤回声明:BIO-1211小分子VLA-4拮抗剂在多发性硬化症EAE小鼠模型中的预防效果。
IF 2.9 4区 医学
Immunological Investigations Pub Date : 2024-11-01 Epub Date: 2024-10-08 DOI: 10.1080/08820139.2024.2412450
{"title":"Statement of Retraction: Prophylactic Effect of BIO-1211 Small-Molecule Antagonist of VLA-4 in the EAE Mouse Model of Multiple Sclerosis.","authors":"","doi":"10.1080/08820139.2024.2412450","DOIUrl":"10.1080/08820139.2024.2412450","url":null,"abstract":"","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1456"},"PeriodicalIF":2.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390315","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
LncRNAPVT1 is Associated with Cancer-Associated Fibroblasts Proliferation Through Regulating TGF-βin Oral Squamous Cell Carcinoma. LncRNAPVT1 通过调节口腔鳞状细胞癌中的 TGF-β 与癌症相关成纤维细胞增殖有关
IF 2.9 4区 医学
Immunological Investigations Pub Date : 2024-11-01 Epub Date: 2024-08-27 DOI: 10.1080/08820139.2024.2395874
Zhen Meng, Tongjuan Li, Jun Li, Shuxin Ding, Yujiao Liu, Guoli Zhao, Cheng Chen, Peng Zhao, Longxun Zhou
{"title":"LncRNAPVT1 is Associated with Cancer-Associated Fibroblasts Proliferation Through Regulating TGF-βin Oral Squamous Cell Carcinoma.","authors":"Zhen Meng, Tongjuan Li, Jun Li, Shuxin Ding, Yujiao Liu, Guoli Zhao, Cheng Chen, Peng Zhao, Longxun Zhou","doi":"10.1080/08820139.2024.2395874","DOIUrl":"10.1080/08820139.2024.2395874","url":null,"abstract":"<p><strong>Introduction: </strong>Human oral squamous cell carcinoma (OSCC) is the most common type of oral cancer and has a poor survival rate. Cell-cell communication between OSCC cells and cancer-associated fibroblasts (CAFs) plays important roles in OSCC progression. We previously demonstrated that CAFs promote OSCC cell migration and invasion. However, how OSCC cells influence CAFs proliferation is unknown.</p><p><strong>Methods: </strong>Knockdown of PVT1 was confirmed using lentivirus infection technique. CAFs in tissues were identified by staining the cells with α-SMA using immunohistochemical technique. CCK-8 assay was used to evaluate cell proliferation. The mRNA level of a gene was measured by qRT-PCR. Secreted TGF-β were detected using ELISA assay.</p><p><strong>Results: </strong>We found that knockdown of the long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) was associated with a low density of CAFs in xenograft tumors in mice; further analysis revealed that PVT1 in OSCC cells induced CAF proliferation through transforming growth factor (TGF)-β.</p><p><strong>Discussion: </strong>Our results demonstrate that lncRNA PVT1 in tumor cells participates in CAF development in OSCC by regulating TGF-β. This study revealed a new mechanism by which PVT1 regulates OSCC progression and PVT1 is a potential therapeutic target in OSCC.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1250-1263"},"PeriodicalIF":2.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072699","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
Soybean Isoflavones Alleviate Osteoarthritis Through Modulation of the TSC1/mTORC1 Signaling Pathway to Reduce Intrachondral Angiogenesis. 大豆异黄酮通过调节 TSC1/mTORC1 信号通路来减少软骨内血管生成,从而缓解骨关节炎。
IF 2.9 4区 医学
Immunological Investigations Pub Date : 2024-11-01 Epub Date: 2024-10-03 DOI: 10.1080/08820139.2024.2410737
Yang Zou, Zhaoyang Wang, Hangchu Shi, Jiong Hu, Weifeng Hu
{"title":"Soybean Isoflavones Alleviate Osteoarthritis Through Modulation of the TSC1/mTORC1 Signaling Pathway to Reduce Intrachondral Angiogenesis.","authors":"Yang Zou, Zhaoyang Wang, Hangchu Shi, Jiong Hu, Weifeng Hu","doi":"10.1080/08820139.2024.2410737","DOIUrl":"10.1080/08820139.2024.2410737","url":null,"abstract":"<p><strong>Background: </strong>The incidence of osteoarthritis (OA) is increasing, yet its pathogenesis remains largely unknown. Recent studies suggest that abnormal subchondral bone remodeling plays a crucial role in OA development, highlighting a gap in clinical treatments targeting this aspect. Soybean Isoflavone (SI) has shown potential in treating OA, although its mechanisms are not fully understood.</p><p><strong>Methods: </strong>This research investigated the effects of SI on subchondral bone remodeling in an OA rat model, assessing joint damage, OARSI scores, and type H vessel formation (CD31hiEmcnhi expression). Additionally, the expression of ALP, OCN, BMP, and TSC1 was evaluated to determine involvement of the mTORC1 pathway. In vitro studies on IL-1β-induced osteoblasts further examined the impact of SI on TSC1/mTORC1 signaling and related markers.</p><p><strong>Results: </strong>SI treatment reduced joint damage and OARSI scores in the rat OA model, significantly decreasing CD31hiEmcnhi expression, indicating a reduction in type H vessel formation. SI also downregulated ALP, OCN, and BMP expression while upregulating TSC1, suggesting inhibition of the mTORC1 signaling pathway and VEGF release. In vitro, SI increased TSC1 expression and decreased mTORC1 signaling, VEGF, ALP, OCN, and BMP levels in IL-1β-induced osteoblasts.</p><p><strong>Conclusion: </strong>SI targets the TSC1/mTORC1 signaling pathway to suppress osteoblast activation and VEGF release, inhibiting type H vessel formation and slowing abnormal subchondral bone remodeling. These findings provide a novel therapeutic approach for OA by focusing on subchondral bone remodeling mechanisms.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1439-1455"},"PeriodicalIF":2.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142365130","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
Resolvin E1 and Inhibition of BLT2 Signaling Attenuate the Inflammatory Response and Improve One-Lung Ventilation-Induced Lung Injury. Resolvin E1 和抑制 BLT2 信号传导可减轻炎症反应并改善单肺通气诱发的肺损伤。
IF 2.9 4区 医学
Immunological Investigations Pub Date : 2024-11-01 Epub Date: 2024-09-04 DOI: 10.1080/08820139.2024.2399587
Liting Ji, Gang Liu, Gongmin Yu, Changxing Xia, Shan Liu, Yunping Lan
{"title":"Resolvin E1 and Inhibition of BLT2 Signaling Attenuate the Inflammatory Response and Improve One-Lung Ventilation-Induced Lung Injury.","authors":"Liting Ji, Gang Liu, Gongmin Yu, Changxing Xia, Shan Liu, Yunping Lan","doi":"10.1080/08820139.2024.2399587","DOIUrl":"10.1080/08820139.2024.2399587","url":null,"abstract":"<p><strong>Introduction: </strong>One-lung ventilation (OLV) is a prevalently used technique to sustain intraoperative pulmonary function. Resolvin E1 (RvE1), a specialized pro-resolving lipid mediator, accelerates the resolution of inflammation in the lungs. However, its therapeutic effects on OLV-induced lung injury remain unclear.</p><p><strong>Methods: </strong>We initially developed an OLV rat model and treated it with RvE1. Subsequently, we assessed the wet/dry ratio of the lung tissue, performed hematoxylin and eosin staining, and calculated the ratio of polymorphonuclear cells to white blood cells in the bronchoalveolar lavage fluid. Additionally, we assessed apoptosis, inflammatory factor levels, and lung permeability in the rat lung tissues in the RvE1 treated and untreated groups and explored the molecular mechanisms mediated by RvE1.</p><p><strong>Results: </strong>Our results indicated that RvE1 alleviated lung injury and inflammation and improved lung tissue apoptosis and permeability in OLV rats. Moreover, RvE1 suppressed the expression of the BLT1/2 signaling pathway and its ligands. The use of BLT2 and BLT1 inhibitors (LY255283 and U-75302, respectively) enhanced RvE1's anti-inflammatory effects and reduced lung injury. Furthermore, synergistic treatment with the BLT2 inhibitor and RvE1 provided grater benefits by more effectively inhibiting the NF-kB, p38 MAPK, and ERK pathways.</p><p><strong>Discussion: </strong>RvE1 and the inhibition of BLT2 signalling reduce the inflammatory response and mitigate OLV-induced lung injury. These findings suggest a novel therapeutic pathway for managing OLV-related complications.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1293-1307"},"PeriodicalIF":2.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142125628","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
Correlation and Clinical Significance of HBD-2 and CXCL-1/2 Levels at Skin Lesions with Psoriasis Vulgaris Severity. 皮损处 HBD-2 和 CXCL-1/2 水平与银屑病严重程度的相关性和临床意义
IF 2.9 4区 医学
Immunological Investigations Pub Date : 2024-11-01 Epub Date: 2024-09-20 DOI: 10.1080/08820139.2024.2395852
Ling Lin, Quan Luo, Xinjing Gao, Qian Li, Wei Li, Xin Zhou, Weiyu Liu, Xuelian Zhong, Yunqing Yang, Xibao Zhang
{"title":"Correlation and Clinical Significance of HBD-2 and CXCL-1/2 Levels at Skin Lesions with Psoriasis Vulgaris Severity.","authors":"Ling Lin, Quan Luo, Xinjing Gao, Qian Li, Wei Li, Xin Zhou, Weiyu Liu, Xuelian Zhong, Yunqing Yang, Xibao Zhang","doi":"10.1080/08820139.2024.2395852","DOIUrl":"10.1080/08820139.2024.2395852","url":null,"abstract":"<p><strong>Objective: </strong>This study was performed to explore the clinical significance of the expression of human beta-defensin 2 (HBD-2) and chemokine ligand 1/2 (CXCL-1/2) in psoriasis vulgaris.</p><p><strong>Methods: </strong>This study retrospectively included the study group (n = 160) and control group (n = 100) for analysis. The levels of inflammatory indicators, blood biochemical indicators, and immune indicators using ELISA. The psoriasis area and severity index (PASI) was used to evaluate disease severity. Levels of HBD-2, CXCL-1, CXCL-2 and CCL20 were determined by RT-PCR. The correlations of HBD-2, CXCL-1 and CXCL-2 levels with CCL20 and PASI scores were analyzed. The diagnostic value of HBD-2, CXCL-1 and CXCL-2 in psoriasis vulgaris was analyzed by ROC curve.</p><p><strong>Results: </strong>HBD-2, CXCL-1 and CXCL-2 were highly expressed in the lesions of psoriasis vulgaris patients, and were positively correlated with CCL20 and PASI score. HBD-2, CXCL-1 and CXCL-2 alone or in combination had high diagnostic value for psoriasis vulgaris and severe psoriasis, and the combined diagnostic value of the three was higher than that of a single indicator.</p><p><strong>Conclusion: </strong>HBD-2, CXCL-1, and CXCL-2 levels are closely related to the severity of psoriasis vulgaris and can effectively diagnose the occurrence and progression of psoriasis vulgaris.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1234-1249"},"PeriodicalIF":2.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286169","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 Identification of Cell Type-Specific Susceptibility Genes for SLE Through the Analysis of RNA Modification-Associated SNPs. 通过分析与 RNA 修饰相关的 SNPs,在全基因组范围内鉴定细胞类型特异的系统性红斑狼疮易感基因。
IF 2.9 4区 医学
Immunological Investigations Pub Date : 2024-11-01 Epub Date: 2024-09-04 DOI: 10.1080/08820139.2024.2399577
Huan Zhang, Kedi Fan, Yuxi Chen, Peng Xu, Zhentao Zhang, Xingbo Mo, Yufan Guo
{"title":"Genome-Wide Identification of Cell Type-Specific Susceptibility Genes for SLE Through the Analysis of RNA Modification-Associated SNPs.","authors":"Huan Zhang, Kedi Fan, Yuxi Chen, Peng Xu, Zhentao Zhang, Xingbo Mo, Yufan Guo","doi":"10.1080/08820139.2024.2399577","DOIUrl":"10.1080/08820139.2024.2399577","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to elucidate the functional genes associated with systemic lupus erythematosus (SLE) in various cell types through the utilization of RNAm-SNPs.</p><p><strong>Methods: </strong>Utilizing large-scale genetic data, we identified associations between RNAm-SNPs and SLE. The association between RNAm-SNPs and bulk and single-cell mRNA expression (eQTL) and protein levels (pQTL) were examined. Mendelian randomization and differential expression analyses were conducted to explore the links between gene expression, protein levels, and SLE.</p><p><strong>Results: </strong>We identified 41 RNAm-SNPs that were significantly associated with SLE. The GWAS signals exhibited notable enrichment in m<sup>6</sup>A-SNPs and m<sup>7</sup>G-SNPs. These RNAm-SNPs showed both eQTL and pQTL effects. In our single-cell analysis, 16 RNAm-SNPs exhibited associations with gene expression levels across 13 distinct cell types, including <i>HLA-A, HLA-B, HLA-C, HLA-DQA1, HLA-DQB1, HLA-DRB1</i> and <i>IRF7</i>. We identified 58 noteworthy associations between the expression levels of 20 genes and SLE across 12 distinct immune cell types. Notably, <i>HLA-DQB1, HLA-DRB1</i> and <i>IRF7</i> exhibited abnormalities in CD8+ T cells, <i>IRF7</i> displayed abnormal expression in CD4+ T cells, while <i>HLA-DRB1</i> and <i>IRF7</i> were also distinctly perturbed in natural killer cells.</p><p><strong>Discussion: </strong>This study advances our understanding of the genetic basis of SLE by highlighting the significance of RNAm-SNPs and immune cell gene expression in SLE.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1264-1278"},"PeriodicalIF":2.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142125627","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
Crosstalk and Prospects of TBK1 in Inflammation. TBK1 在炎症中的相互作用与前景
IF 2.9 4区 医学
Immunological Investigations Pub Date : 2024-11-01 Epub Date: 2024-08-28 DOI: 10.1080/08820139.2024.2392587
Huan Liu, Qihuan Sheng, Juhua Dan, Xiaoli Xie
{"title":"Crosstalk and Prospects of TBK1 in Inflammation.","authors":"Huan Liu, Qihuan Sheng, Juhua Dan, Xiaoli Xie","doi":"10.1080/08820139.2024.2392587","DOIUrl":"10.1080/08820139.2024.2392587","url":null,"abstract":"<p><strong>Background: </strong>TANK-binding kinase 1 (TBK1) is a pivotal mediator of innate immunity, activated by receptors such as mitochondrial antiviral signaling protein (MAVS), stimulator of interferon genes (STING), and TIR-domain-containing adaptor inducing interferon-β (TRIF). It modulates immune responses by exerting influence on the type I interferons (IFN-Is) signaling and the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathways, Over the past few years, TBK1 multifaceted role in both immune and inflammatory responses is increasingly recognized.</p><p><strong>Methods and results: </strong>This review aims to scrutinize how TBK1 operates within the NF-κB pathway and the interferon regulatory transcription factor 3 (IRF3)-dependent IFN-I pathways, highlighting the kinases and other molecules involved in these processes. This analysis reveals the distinctive characteristics of TBK1's involvement in these pathways. Furthermore, it has been observed that the role of TBK1 in exerting anti-inflammatory or pro-inflammatory effects is contingent upon varying pathological conditions, indicating a multifaceted role in immune regulation.</p><p><strong>Discussion: </strong>TBK1's evolving role in various diseases and the potential of TBK1 inhibitors as therapeutic agents are explored. Targeting TBK1 may provide new strategies for treating inflammatory disorders and autoimmune diseases associated with IFN-Is, warranting further investigation.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1205-1233"},"PeriodicalIF":2.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142080190","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
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