Autoimmunity最新文献_第4页

Animal models of immune-mediated demyelinating polyneuropathies. 免疫介导的脱髓鞘性多发性神经病的动物模型。

IF 3.3 4区医学

Autoimmunity Pub Date : 2024-12-01 Epub Date: 2024-06-08 DOI: 10.1080/08916934.2024.2361745

Eroboghene E Ubogu

{"title":"Animal models of immune-mediated demyelinating polyneuropathies.","authors":"Eroboghene E Ubogu","doi":"10.1080/08916934.2024.2361745","DOIUrl":"10.1080/08916934.2024.2361745","url":null,"abstract":"Immune-mediated demyelinating polyneuropathies (IMDPs) are rare disorders in which dysregulated adaptive immune responses cause peripheral nerve demyelinating inflammation and axonal injury in susceptible individuals. Despite significant advances in understanding IMDP pathogenesis guided by patient data and representative mammalian models, specific therapies are lacking. Significant knowledge gaps in IMDP pathogenesis still exist, e.g. precise antigen(s) and mechanisms that initially trigger immune system activation and identification of large population disease susceptibility factors. The initial directional cues for antigen-specific effector or autoreactive leukocyte trafficking into peripheral nerves are also unknown. An overview of current animal models, with emphasis on the experimental autoimmune neuritis and spontaneous autoimmune peripheral polyneuropathy models, is provided. Insights on the initial directional cues for peripheral nerve tissue specific autoimmunity using a novel Major Histocompatibility Complex class II conditional knockout mouse strain are also discussed, suggesting an essential research tool to study cell- and time-dependent adaptive immunity in autoimmune diseases.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"57 1","pages":"2361745"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11215812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141293055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Osteocyte-derived exosomes regulate the DLX2/wnt pathway to alleviate osteoarthritis by mediating cartilage repair. 骨细胞源性外泌体调节 DLX2/wnt 通路，通过介导软骨修复缓解骨关节炎。

IF 3.3 4区医学

Autoimmunity Pub Date : 2024-12-01 Epub Date: 2024-07-01 DOI: 10.1080/08916934.2024.2364686

Wenjuan Xu, Yuanyuan Zhang, Lijuan Li, Liyan Pan, Li Lu, Shenshen Zhi, Wei Li

{"title":"Osteocyte-derived exosomes regulate the DLX2/wnt pathway to alleviate osteoarthritis by mediating cartilage repair.","authors":"Wenjuan Xu, Yuanyuan Zhang, Lijuan Li, Liyan Pan, Li Lu, Shenshen Zhi, Wei Li","doi":"10.1080/08916934.2024.2364686","DOIUrl":"10.1080/08916934.2024.2364686","url":null,"abstract":"Background: Chondrocyte viability, apoptosis, and migration are closely related to cartilage injury in osteoarthritis (OA) joints. Exosomes are identified as potential therapeutic agents for OA.Objective: This study aimed to investigate the role of exosomes derived from osteocytes in OA, particularly focusing on their effects on cartilage repair and molecular mechanisms.Methods: An injury cell model was established by treating chondrocytes with IL-1β. Cartilage repair was evaluated using cell counting kit-8, flow cytometry, scratch test, and Western Blot. Molecular mechanisms were analyzed using quantitative real-time PCR, bioinformatic analysis, and Western Blot. An OA mouse model was established to explore the role of exosomal DLX2 in vivo.Results: Osteocyte-released exosomes promoted cell viability and migration, and inhibited apoptosis and extracellular matrix (ECM) deposition. Moreover, exosomes upregulated DLX2 expression, and knockdown of DLX2 activated the Wnt pathway. Additionally, exosomes attenuated OA in mice by transmitting DLX2.Conclusion: Osteocyte-derived exosomal DLX2 alleviated IL-1β-induced cartilage repair and inactivated the Wnt pathway, thereby alleviating OA progression. The findings suggested that osteocyte-derived exosomes may hold promise as a treatment for OA.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"57 1","pages":"2364686"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141465883","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

Subchronic intranasal lipopolysaccharide exposure induces pulmonary autoimmunity and glomerulonephritis in NZBWF1 mice. 亚慢性鼻内脂多糖暴露诱导 NZBWF1 小鼠肺部自身免疫和肾小球肾炎。

IF 3.3 4区医学

Autoimmunity Pub Date : 2024-12-01 Epub Date: 2024-07-08 DOI: 10.1080/08916934.2024.2370536

Lauren K Heine, Lichchavi D Rajasinghe, James G Wagner, Ryan P Lewandowski, Quan-Zhen Li, Alexa L Richardson, Ashleigh N Tindle, Jenan J Shareef, Jack R Harkema, James J Pestka

{"title":"Subchronic intranasal lipopolysaccharide exposure induces pulmonary autoimmunity and glomerulonephritis in NZBWF1 mice.","authors":"Lauren K Heine, Lichchavi D Rajasinghe, James G Wagner, Ryan P Lewandowski, Quan-Zhen Li, Alexa L Richardson, Ashleigh N Tindle, Jenan J Shareef, Jack R Harkema, James J Pestka","doi":"10.1080/08916934.2024.2370536","DOIUrl":"10.1080/08916934.2024.2370536","url":null,"abstract":"Lupus, a systemic autoimmune disease shaped by gene-environment interplay, often progresses to endstage renal failure. While subchronic systemic exposure to bacterial lipopolysaccharide (LPS) triggers autoimmunity and glomerulonephritis in lupus-prone mice, it is unknown if inhaling LPS, which is common in certain occupations, can similarly trigger lupus. Here we determined how subchronic intranasal (IN) LPS instillation influences autoimmunity and glomerulonephritis development in lupusprone NZBWF1 female mice. Briefly, mice were IN-instilled with vehicle or E. coli LPS (0.8 μg/g) twice weekly for 5 wk, followed by necropsy. For systemic comparison, additional cohorts of mice were injected with LPS intraperitoneally (IP) using identical doses/timing. Lungs were assessed for inflammatory and autoimmune responses and then related to systemic autoimmunity and glomerulonephritis. IN/LPS exposure induced in the lung: i) leukocyte infiltration, ii)mRNA signatures for cytokines, chemokines, IFN-regulated, and cell death-related genes, iii) ectopic lymphoid tissue formation, and iv)diverse IgM and IgG autoantibodies (AAbs). Pulmonary effects coincided with enlarged spleens, elevated plasma IgG AAbs, and inflamed IgG-containing kidney glomeruli. In contrast, IP/LPS treatment induced systemic autoimmunity and glomerulonephritis without pulmonary manifestations. Taken together, these preclinical findings suggest the lung could serve as a critical nexus for triggering autoimmunity by respirable LPS in genetically predisposed individuals.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"57 1","pages":"2370536"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11289745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141557935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CircNRIP1 promotes proliferation, migration and phenotypic switch of Ang II-induced HA-VSMCs by increasing CXCL5 mRNA stability via recruiting IGF2BP1. CircNRIP1 通过招募 IGF2BP1 增加 CXCL5 mRNA 的稳定性，从而促进 Ang II 诱导的 HA-VSMC 的增殖、迁移和表型转换。

IF 3.5 4区医学

Autoimmunity Pub Date : 2024-12-01 Epub Date: 2024-01-25 DOI: 10.1080/08916934.2024.2304820

Xianzhao Cao, Hongyan Fang, Longshu Zhou

{"title":"CircNRIP1 promotes proliferation, migration and phenotypic switch of Ang II-induced HA-VSMCs by increasing CXCL5 mRNA stability via recruiting IGF2BP1.","authors":"Xianzhao Cao, Hongyan Fang, Longshu Zhou","doi":"10.1080/08916934.2024.2304820","DOIUrl":"10.1080/08916934.2024.2304820","url":null,"abstract":"Circular RNA (circRNA) has been found to be differentially expressed and involved in regulating the processes of human diseases, including thoracic aortic dissection (TAD). However, the role and mechanism of circNRIP1 in the TAD process are still unclear. GEO database was used to screen the differentially expressed circRNA and mRNA in type A TAD patients and age-matched normal donors. Angiotensin II (Ang II)-induced human aortic vascular smooth muscle cells (HA-VSMCs) were used to construct TAD cell models. The expression levels of circNRIP1, NRIP1, CXC-motif chemokine 5 (CXCL5) and IGF2BP1 were detected by quantitative real-time PCR. Cell proliferation and migration were determined by EdU assay, transwell assay and wound healing assay. The protein levels of synthetic phenotype markers, contractile phenotype markers, CXCL5 and IGF2BP1 were tested by western blot analysis. The interaction between IGF2BP1 and circNRIP1/CXCL5 was confirmed by RIP assay, and CXCL5 mRNA stability was assessed by actinomycin D assay. CircNRIP1 was upregulated in TAD patients and Ang II-induced HA-VSMCs. Knockdown of circNRIP1 suppressed Ang II-induced proliferation, migration and phenotypic switch of HA-VSMCs. Also, high expression of CXCL5 was observed in TAD patients, and its knockdown could inhibit Ang II-induced HA-VSMCs proliferation, migration and phenotypic switch. Moreover, CXCL5 overexpression reversed the regulation of circNRIP1 knockdown on Ang II-induced HA-VSMCs functions. Mechanistically, circNRIP1 could competitively bind to IGF2BP1 and subsequently enhance CXCL5 mRNA stability. CircNRIP1 might contribute to TAD progression by promoting CXCL5 mRNA stability via recruiting IGF2BP1.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"57 1","pages":"2304820"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139544636","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 lupus nephritis: the past, present and a future outlook. 狼疮肾炎的动物模型：过去、现在和未来展望。

IF 3.5 4区医学

Autoimmunity Pub Date : 2024-12-01 Epub Date: 2024-03-13 DOI: 10.1080/08916934.2024.2319203

Divya Katikaneni, Laurence Morel, Yogesh Scindia

引用次数: 0

FOXO3 as a potential diagnostic biomarker for autophagy in rheumatoid arthritis: A bioinformatics study. FOXO3 作为类风湿性关节炎自噬的潜在诊断生物标志物：生物信息学研究

IF 3.3 4区医学

Autoimmunity Pub Date : 2024-12-01 Epub Date: 2024-11-05 DOI: 10.1080/08916934.2024.2423759

Qian Deng, Zining Peng, Fanyu Meng, Wangxin Zeng, Mengyuan Zhu, Nian Liu, Weitian Yan, Jiangyun Peng

{"title":"FOXO3 as a potential diagnostic biomarker for autophagy in rheumatoid arthritis: A bioinformatics study.","authors":"Qian Deng, Zining Peng, Fanyu Meng, Wangxin Zeng, Mengyuan Zhu, Nian Liu, Weitian Yan, Jiangyun Peng","doi":"10.1080/08916934.2024.2423759","DOIUrl":"10.1080/08916934.2024.2423759","url":null,"abstract":"This study aimed to identify genes associated with autophagy and potential diagnostic biomarkers by comparing the gene expression profiles of synovial tissues in patients with rheumatoid arthritis (RA) and healthy individuals, aiming to offer new insights for clinical treatment strategies. We used publicly available datasets to analyze differentially expressed genes (DEGs) between the synovial tissue of RA patients and healthy individuals. Then, we intersected these DEGs with autophagy-related genes to identify autophagy genes in the synovial tissue of RA patients. We further analyzed the biological processes and functions of these genes. Furthermore, we used machine learning to identify characteristic autophagy genes in RA synovial tissue. Finally, we examined the differential expression of these characteristic genes in the blood of RA patients using an external dataset. Our study identified FOXO3 as a potential biomarker for diagnosing RA. FOXO3 gene expression was downregulated in both the synovial tissue and blood of RA patients, suggesting its involvement in multiple biological processes such as local inflammation, oxidative stress, metabolic processes, and immune responses. Our findings suggest that FOXO3 may be a novel biomarker for the clinical diagnosis of RA and may play a crucial role in the pathogenesis of RA. The study provides new insights into the molecular mechanisms of RA and potential new therapeutic targets.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"57 1","pages":"2423759"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142575142","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

The role of gut microbiota in different murine models of systemic lupus erythematosus. 肠道微生物群在不同的系统性红斑狼疮小鼠模型中的作用。

IF 3.3 4区医学

Autoimmunity Pub Date : 2024-12-01 Epub Date: 2024-07-16 DOI: 10.1080/08916934.2024.2378876

Ran Lu, Xin M Luo

引用次数: 0

Identification of new hub- ferroptosis-related genes in Lupus Nephritis. 鉴定狼疮性肾炎中新的枢纽型铁变态反应相关基因

IF 3.5 4区医学

Autoimmunity Pub Date : 2024-12-01 Epub Date: 2024-02-26 DOI: 10.1080/08916934.2024.2319204

Xiao-Jie Zheng, Ying Chen, Li Yao, Xiao-Li Li, Da Sun, Yan-Qiu Li

{"title":"Identification of new hub- ferroptosis-related genes in Lupus Nephritis.","authors":"Xiao-Jie Zheng, Ying Chen, Li Yao, Xiao-Li Li, Da Sun, Yan-Qiu Li","doi":"10.1080/08916934.2024.2319204","DOIUrl":"10.1080/08916934.2024.2319204","url":null,"abstract":"Background: Lupus Nephritis (LN) is the primary causation of kidney injury in systemic lupus erythematosus (SLE). Ferroptosis is a programmed cell death. Therefore, understanding the crosstalk between LN and ferroptosis is still a significant challenge. Methods: We obtained the expression profile of LN kidney biopsy samples from the Gene Expression Omnibus database and utilised the R-project software to identify differentially expressed genes (DEGs). Then, we conducted a functional correlation analysis. Ferroptosis-related genes (FRGs) and differentially expressed genes (DEGs) crossover to select FRGs with LN. Afterwards, we used CIBERSORT to assess the infiltration of immune cells in both LN tissues and healthy control samples. Finally, we performed immunohistochemistry on LN human renal tissue. Results: 10619 DEGs screened from the LN biopsy tissue were identified. 22 hub-ferroptosis-related genes with LN (FRGs-LN) were screened out. The CIBERSORT findings revealed that there were significant statistical differences in immune cells between healthy control samples and LN tissues. Immunohistochemistry further demonstrated a significant difference in HRAS, TFRC, ATM, and SRC expression in renal tissue between normal and control groups. Conclusion: We developed a signature that allowed us to identify 22 new biomarkers associated with FRGs-LN. These findings suggest new insights into the pathology and therapeutic potential of LN ferroptosis inhibitors and iron chelators.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"57 1","pages":"2319204"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139970769","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

Functions of IgM fc receptor (FcµR) related to autoimmunity. 与自身免疫有关的 IgM fc 受体（FcµR）的功能。

IF 3.5 4区医学

Autoimmunity Pub Date : 2024-12-01 Epub Date: 2024-03-11 DOI: 10.1080/08916934.2024.2323563

Hiromi Kubagawa, Pedram Mahmoudi Aliabadi, Khlowd Al-Qaisi, Peter K Jani, Kazuhito Honjo, Shozo Izui, Andreas Radbruch, Fritz Melchers

引用次数: 0

Animal models of neuropsychiatric systemic lupus erythematosus: deciphering the complexity and guiding therapeutic development. 神经精神系统性红斑狼疮的动物模型：解读复杂性并指导治疗开发。

IF 3.5 4区医学

Autoimmunity Pub Date : 2024-12-01 Epub Date: 2024-03-31 DOI: 10.1080/08916934.2024.2330387

Baruh Polis, Carla M Cuda, Chaim Putterman

{"title":"Animal models of neuropsychiatric systemic lupus erythematosus: deciphering the complexity and guiding therapeutic development.","authors":"Baruh Polis, Carla M Cuda, Chaim Putterman","doi":"10.1080/08916934.2024.2330387","DOIUrl":"10.1080/08916934.2024.2330387","url":null,"abstract":"Systemic lupus erythematosus (SLE) poses formidable challenges due to its multifaceted etiology while impacting multiple tissues and organs and displaying diverse clinical manifestations. Genetic and environmental factors contribute to SLE complexity, with relatively limited approved therapeutic options. Murine models offer insights into SLE pathogenesis but do not always replicate the nuances of human disease. This review critically evaluates spontaneous and induced animal models, emphasizing their validity and relevance to neuropsychiatric SLE (NPSLE). While these models undoubtedly contribute to understanding disease pathophysiology, discrepancies persist in mimicking some NPSLE intricacies. The lack of literature addressing this issue impedes therapeutic progress. We underscore the urgent need for refining models that truly reflect NPSLE complexities to enhance translational fidelity. We encourage a comprehensive, creative translational approach for targeted SLE interventions, balancing scientific progress with ethical considerations to eventually improve the management of NPSLE patients. A thorough grasp of these issues informs researchers in designing experiments, interpreting results, and exploring alternatives to advance NPSLE research.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"57 1","pages":"2330387"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140331540","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