Immunity, Inflammation and Disease最新文献

{"title":"The Role of Persistent Inflammation in the Pathogenesis of Infected Nonunion: A Narrative Review","authors":"Tao Liu,&nbsp;Fengjiang Li,&nbsp;Yuanbin Yan,&nbsp;Silong Gao,&nbsp;Daqian Zhou,&nbsp;Xuanang Jiang,&nbsp;Chao Song,&nbsp;Zhijiang Fu,&nbsp;Zongchao Liu","doi":"10.1002/iid3.70260","DOIUrl":"10.1002/iid3.70260","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Infected Nonunion is a challenging condition that arises from infections at the fracture site, causing persistent inflammation and preventing proper healing of the fracture ends. This condition not only causes significant physical suffering but also imposes a heavy economic burden on patients. Despite the recognized link between Infected Nonunion and infection, the mechanisms underlying its occurrence and development remain incompletely understood. Recent studies have highlighted the close association between inflammatory factors and Infected Nonunion, suggesting that inflammation plays a pivotal role in its pathogenesis. However, a narrative review and summary of relevant literature are lacking. Therefore, this study aims to clarify the inflammatory mechanisms of Infected Nonunion and identify potential therapeutic targets.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A comprehensive literature search was conducted to identify relevant domestic and international studies on the inflammatory mechanisms of Infected Nonunion. The search included databases such as PubMed using keywords related to Infected Nonunion, inflammation, and mechanisms. The selected studies were critically reviewed and summarized to extract key information on the inflammatory pathways, cytokines, and other relevant factors involved in Infected Nonunion.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The review identified several key inflammatory mechanisms that contribute to the development of Infected Nonunion. These include the activation of inflammatory cells, the release of inflammatory cytokines and chemokines, and the disruption of normal fracture healing processes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This narrative review elucidates novel perspectives on the inflammatory mechanisms in infected nonunion, with persistent inflammatory response triggered by pathogenic infection representing the core pathological process. The findings provide theoretical foundations for future research and therapeutic strategies, potentially facilitating the development of more effective treatments for infected nonunion. Targeted modulation of these inflammatory pathways may optimize fracture healing outcomes and alleviate the clinical burden of this condition.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 9","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12439192/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069451","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}

{"title":"Correction to “TFRC in Cardiomyocytes Promotes Macrophage Infiltration and Activation During the Process of Heart Failure Through Regulating Ccl2 Expression Mediated by Hypoxia Inducible Factor-1Α”","authors":"","doi":"10.1002/iid3.70262","DOIUrl":"10.1002/iid3.70262","url":null,"abstract":"<p>Pan Y, Yang J, Dai J, Xu X, Zhou X, Mao W. TFRC in cardiomyocytes promotes macrophage infiltration and activation during the process of heart failure through regulating Ccl2 expression mediated by hypoxia inducible factor-1α. Immunity, Inflammation and Disease 2023; 11:e835. doi:10.1002/iid3.835</p><p>In the “Figure Legend” section of Figure 1B, the text “The bar is 50 μm.” was incorrect. This should have read: “The bar of the left-hand panel is 50 μm. The right-hand panel depicts a magnified view of selected regions from the left-hand images, with the bar of 100 μm.”. In the “Figure Legend” section of Figure 1C, the annotation of Crosses was inadvertently omitted. This should have read: (C) The correlation analysis of different cells in HF tissue. The right-side vertical bar chart employs a gradient color scale (red to blue) to quantify correlation strength, with red indicating positive and blue negative correlations. The y-axis spans from −1 to 1, where the single bar reaching maximum amplitude (value = 1) demonstrates the strongest positive correlation. The visual hierarchy is further clarified by: (1) Circular markers whose size corresponds to absolute correlation magnitude; (2) Cross symbols denoting statistical insignificance. In the “Figure Legend” section of Figure 1D, the annotation of the x-axis was inadvertently omitted. This should have read: (D) The correlation analysis of TFRC expression and different cells in HF tissue (CM, cardiomyocytes; EC, endothelial cells; FB, fibroblasts; MP, macrophages; GN, neutrophile granulocyte; T, T cells). The x-axis represents the relative mRNA expression level of TFRC, while the y-axis illustrates the corresponding cell population proportions. The authors also admitted to an image compilation error in the subpanels of Figure 1B and were able to provide the original images. The authors confirm that all the experimental results and corresponding conclusions mentioned in the paper remain unaffected. The corrected Figure 1 is shown as follows.</p><p>Corrected Figure 1</p><p>The authors apologize for these errors.</p>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 9","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70262","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032647","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}

{"title":"Correction to “Downregulation of BIRC2 Hinders the Progression of Rheumatoid Arthritis Through Regulating TRADD]”","authors":"","doi":"10.1002/iid3.70261","DOIUrl":"10.1002/iid3.70261","url":null,"abstract":"<p>Y. Rao, S. Xu, T. Lu, Y. Wang, M. Liu and W. Zhang, “Downregulation of BIRC2 hinders the progression of rheumatoid arthritis through regulating TRADD”, <i>Immunity, Inflammation and Disease</i>, no. 11 (2023): e978, https://doi.org/10.1002/iid3.978.</p><p>In paragraph 4 of the Materials and Methods section, the sequence information of si-BIRC-1 and si-BIRC2 is missing. This should be modified as follows: For the BIRC2 knockdown, the small interfering RNA (siRNA) targeting BIRC2 (si-BIRC2-1 (5′-CAGGGCTTTAAGTTAGTATTA-3′) and si-BIRC2-2 (5′-TAGGCGTTTCTGATAACACTA-3′)) were constructed by GenePharma (Shanghai, China).</p><p>The authors apologize for this omission.</p>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 9","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70261","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032667","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}

{"title":"Safety and 1-Year Outcomes After Transplanting Hearts From SARS-CoV-2 Positive Donors: Insights From an International Analysis","authors":"Sabina P. W. Guenther,&nbsp;Josephine Wadewitz,&nbsp;Brian J. Wayda,&nbsp;Henrik Fox,&nbsp;Rayan Cheaban,&nbsp;Yasuhiro Shudo,&nbsp;William Hiesinger,&nbsp;Angelika Costard-Jäckle,&nbsp;Michiel Morshuis,&nbsp;Y. Joseph Woo,&nbsp;Jeffrey J. Teuteberg,&nbsp;René Schramm,&nbsp;Axel Rahmel,&nbsp;Jan F. Gummert,&nbsp;Kiran K. Khush","doi":"10.1002/iid3.70252","DOIUrl":"https://doi.org/10.1002/iid3.70252","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Uncertainties persist regarding the utilization of hearts from SARS-CoV-2-positive donors for heart transplant (HT). This international study analyzed such HTs within the United States (US) and Germany, focusing on 1-year outcomes and granular safety data.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Data was obtained from the United Network for Organ Sharing (UNOS) registry (03/2021–08/2022) and collaborating with the German Organ Procurement Organisation (DSO; 03/2022–02/2023). HTs from currently and recently (up to 21 days in UNOS and 90 days in DSO) SARS-CoV-2-positive donors were included.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In the US, 274 HTs from SARS-CoV-2 donors were analyzed (50.7% SARS-CoV-2-positive until organ recovery). Compared to 3952 HTs from SARS-CoV-2-negative donors, acute rejection was less frequent (10.6% vs. 17.1%, <i>p</i> = 0.006). One-year graft and recipient survival (<i>p</i> = 0.327) and rehospitalization rates (<i>p</i> = 0.592) did not differ. In Germany, 30 HTs utilized SARS-CoV-2-positive hearts. Follow-up was obtained for 23 (76.7%). 43.5% of the donors were positive until recovery. Two recipients (8.7%) tested positive for SARS-CoV-2 21 and 65 days post-transplant, both unlikely donor-derived. 8.7% had severe PGD, 8.7% acute cellular rejection ≥ 2R. One-year survival was 91.3%. None experienced myocarditis or thromboembolism.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Using selected SARS-CoV-2-positive hearts for transplant appears safe with no differences in 1-year survival, no evidence of viral transmission or SARS-CoV-2-related adverse cardiovascular events.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 9","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70252","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144997953","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}

{"title":"Circadian Clock: A Regulator of Immunity in Autoimmune Diseases","authors":"Ye-Jun Wu,&nbsp;Shu-Ying Zhang,&nbsp;Hong-Yu Chen,&nbsp;Xin-Ran He,&nbsp;Guang-Rui Yang","doi":"10.1002/iid3.70246","DOIUrl":"https://doi.org/10.1002/iid3.70246","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Autoimmune diseases, characterized by the immune system mistakenly attacking the body's own tissues, are a growing global concern, with increasing prevalence. The circadian clock is a fundamental regulator of physiological processes, critically modulating immune functions. This review explores the intricate connections between circadian rhythms and immune responses in autoimmune pathogenesis and how disruptions exacerbate disease.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This synthesis examines recent research on circadian regulation of immune functions (leukocyte trafficking, cytokine secreion, phagocytosis) and autoimmune progression. Key evidence includes roles of core clock proteins such as brain and muscle ARNT-Like 1 (BMAL1), circadian locomotor output cycles kaput (CLOCK), and REV-ERBα, along with circadian-regulated immune cells, and impacts of environmental/lifestyle-induced circadian disruption.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Ciradian rhythms significantly influence autoimmune disease progression and symptom patterns (e.g., morning joint stiffness in rheumatoid arthritis). Core clock proteins and rhythmic immune cells are critical for homeostasis. Circadian disruptions exacerbate immune dysfunction, promoting chronic inflammation and autoimmunity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The circadian clock is a fundamental regulator of immune function and autoimmune pathogenesis. Disruption worsens disease progression. Understanding these mechanisms opens new avenues for therapeutic interventions, including chronotherapy and targeting clock genes, with the potential to improve treatment outcomes in autoimmune diseases.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 9","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70246","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144997952","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}

{"title":"Assessing the Efficacy and Immunogenicity of Anticaries Vaccine—A Systematic Review and Meta-Analysis","authors":"Gunjan Kumar,&nbsp;Payal Dash,&nbsp;Smruti Bhusan Nanda,&nbsp;Mohammad Fareed,&nbsp;Mohmed Isaqali Karobari","doi":"10.1002/iid3.70253","DOIUrl":"https://doi.org/10.1002/iid3.70253","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>The current systematic review and meta-analysis aims to assess the safety and immunogenicity of the anticaries vaccines currently available.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>Electronic searches of PubMed, Scopus, Web of Science and Science Direct were performed. Studies assessing the safety and effectiveness of the anticaries vaccination, including the dose, plasmids, serum IgG and IgA levels after immunization, were included. Studies in which animals were used for anticaries vaccine were also included. Combining more than one trial was done to estimate the pooled intervention effect using the meta-analysis when studies examined the same intervention and outcomes with comparable methods in similar populations. The continuous data was pooled using the inverse variance method, and dichotomous data using the Mantel-Haenszel method.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Out of 4701 records, only 17 publications met the eligibility criteria. Although all studies were assessed as having an overall low risk of bias, certain domains (D3, D5, and D7) exhibited a high risk across most studies. The pooled RR, derived using a random-effects model, was 0.53 (95% CI: 0.46–0.62), indicating a statistically significant 47% reduction in risk across studies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>There is excellent potential for dental caries vaccines to transform oral health in the future. Various vaccines, such as Killed Formalin-treated Donor strain 2 - recombinant Protein Antigen c and anti-CAT-SYIIgY antibodies, have demonstrated prophylactic effects against Streptococcus mutans colonization on teeth. These interventions exhibit a sustained reduction in S. mutans colonization, which may contribute to the prevention of dental caries. A vaccination of this kind would significantly lower tooth decay prevalence and the financial and health costs that go along with it.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 9","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70253","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144997954","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}

{"title":"Role and Mechanism of Microglia in White Matter Injury Recovery in Ischemic Stroke","authors":"Yi-Sha Guo,&nbsp;Yunlin Shang,&nbsp;Jiajia Yao,&nbsp;Xia Bi","doi":"10.1002/iid3.70226","DOIUrl":"https://doi.org/10.1002/iid3.70226","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Ischemic stroke frequently leads to white matter injury (WMI), significantly impairing neurological function and recovery. Microglia, the central nervous system's resident immune cells, play a dual role in poststroke pathology and repair. Their diverse activation states and interactions with other glial cells influence demyelination, remyelination, and overall WMI outcomes. To systematically review and synthesize the current evidence regarding the temporal and functional dynamics of microglia in ischemic stroke, with a focus on their roles in white matter damage and recovery.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A comprehensive literature search was conducted using PubMed, Web of Science, and Scopus databases (through December 2024) with keywords including “ischemic stroke,” “white matter injury,” “microglia,” “myelin,” and “oligodendrocytes.” Studies involving mechanistic insights into microglial polarization, myelin repair, and associated molecular pathways were prioritized. Both preclinical and clinical studies were reviewed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Microglia exhibit distinct activation profiles in acute and chronic phases poststroke. Pro-inflammatory microglia exacerbate WMI via cytokine secretion and oligodendrocyte toxicity, while immune-regulatory microglia promote remyelination through trophic support and debris clearance. Key regulatory pathways include TREM2, CX3CR1, and purinergic signaling. Microglial phagocytosis, cytokine production, and interactions with astrocytes critically modulate remyelination. Therapeutic modulation of microglial phenotype (e.g., fingolimod, HDAC inhibitors) shows promise in enhancing white matter repair.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Microglia exert time- and region-specific effects on WMI after ischemic stroke. A nuanced understanding of their dynamic phenotypes and interactions with other glial elements is essential for developing targeted therapies. Future research should integrate single-cell technologies, human validation, and sex-specific analyses to refine microglia-based interventions.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70226","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144910404","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}

{"title":"Vascular Smooth Muscle-Secreted Exosomal X26nt Impedes Atherosclerosis Progression via the c-FOS/XBP1/SOD1 Axis","authors":"Zhibin Zhang,&nbsp;Dachang Liu,&nbsp;Yue Zheng,&nbsp;Yanwu Liu,&nbsp;Xian Cheng,&nbsp;Yun Chang,&nbsp;Xiaoyu Liang,&nbsp;Xiaomin Hu,&nbsp;Wenqing Gao","doi":"10.1002/iid3.70251","DOIUrl":"https://doi.org/10.1002/iid3.70251","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Atherosclerosis is a chronic immune-inflammatory disorder in which vascular smooth muscle cell (VSMC) phenotypic modulation plays a critical role in plaque development and instability. Endoplasmic reticulum (ER) stress and its downstream effector, XBP1s, have been shown to influence VSMC behavior. During XBP1 mRNA splicing, a 26-nucleotide RNA fragment (X26nt) is excised, yet its biological significance remains poorly understood. Exosomes derived from VSMCs have been implicated in mediating intercellular signaling under inflammatory and stress conditions. However, the potential role of X26nt in vascular regulation, particularly via exosomal pathways, has not been investigated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Atherosclerosis was induced in ApoE-/- mice using a high-fat diet. Ox-LDL-treated VSMCs were used for in vitro studies. Histology, qPCR, and Western blot were conducted. Exosomes from IRE1α- or XBP1-knockdown VSMCs were isolated and used to treat Ox-LDL-exposed VSMCs to assess X26nt effects. Luciferase assays and ChIP were used to explore mechanisms. AAV2-SM22a-ZsGreen-26nt vectors were constructed to evaluate X26nt effects in vivo.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>X26nt levels in exosomes increased with arterial medial thickening in atherosclerosis. In vitro, exosomal X26nt decreased ER stress, suppressed mitophagy, and upregulated SOD1 in VSMCs. Exosomes from IRE1α- or XBP1-knockdown VSMCs reversed the protective phenotype. Mechanistically, X26nt bound the 3'UTR of XBP1 and c-Fos, reducing their expression. ChIP confirmed c-Fos directly activated XBP1 transcription. In vivo, AAV2-X26nt delivery elevated SOD1, reduced mitophagy, and attenuated vascular remodeling.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study identified exosomal X26nt as a novel regulator of VSMC phenotypic switching and oxidative stress through the c-Fos/XBP1/SOD1 axis. These findings highlight the functional relevance of ER stress-derived noncoding RNAs in vascular remodeling and suggest that targeting exosomal RNAs, such as X26nt, may represent a promising therapeutic strategy for atherosclerosis and related cardiovascular diseases.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70251","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144897773","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}

{"title":"Carbon Monoxide Alleviates Cardiomyocyte Pyroptosis in Diabetic Cardiomyopathy by Downregulating the IL-33/ST2L Axis","authors":"Chunjie Jiang,&nbsp;Ping Zhu,&nbsp;Ping Yao,&nbsp;Xiaojun Bi,&nbsp;Chao Gao","doi":"10.1002/iid3.70231","DOIUrl":"https://doi.org/10.1002/iid3.70231","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>This study aimed to investigate whether carbon monoxide (CO) can alleviate cardiomyocyte pyroptosis by downregulating the IL-33/ST2L axis in diabetic cardiomyopathy (DCM).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The diabetic mouse model was established and treated with CO-releasing molecule-2 (CORM-2) or invalid CORM-2 (iCORM-2). For in vitro studies, cardiomyocytes were treated with high glucose (HG).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The HG-treated cardiomyocytes exhibited increased IL-33, ST2L, and pyroptosis-related protein expression compared with that in the control group (<i>p</i> &lt; 0.05). Treatment with recombinant IL-33 further increased the expression of HG-induced pyroptosis-related proteins (<i>p</i> &lt; 0.05). Compared with control mice, DCM mice showed reduced cardiac function and elevated expression of IL-33, ST2L, and pyroptosis-related proteins (<i>p</i> &lt; 0.01). Intervention with CORM-2 ameliorated cardiac injury, and decreased the expression of IL-33, ST2L, and pyroptosis-related proteins in vivo and in vitro (<i>p</i> &lt; 0.05). However, iCORM-2 had no effect both in vivo and in vitro.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>In conclusion, CO may inhibit cardiomyocyte pyroptosis by downregulating the IL-33/ST2L axis in DCM mice.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70231","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144892503","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}

{"title":"Development of Thymic Organoids Heterotopically to Educate and Induce T Lymphocytes","authors":"Xiuxia Wang,&nbsp;Shun Yu,&nbsp;Yucheng Qiu,&nbsp;Jun Yang,&nbsp;Fei Liu,&nbsp;Xianyu Zhou","doi":"10.1002/iid3.70229","DOIUrl":"https://doi.org/10.1002/iid3.70229","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Vascularized composite allotransplantation (VCA) is a potential treatment for extensive injuries that replaces defects like-with-like, however allografts are immune-rejectable.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This study developed in vitro thymic organoids and examined whether donor-derived HSCs could be educated in vivo into T lymphocytes via central tolerance. TECs, TMCs, and HSCs from C57BL/7 (CD45.2⁺) or SJL/L (CD45.1⁺) mice were labeled with cell surface markers and examined by flow cytometry. Co-culturing three cell lines in vitro created thymic aggregates. Aggregates transplanted to C57BL/7 (CD45.2⁺) mice′s inguinal regions developed thymic organoids. Immunorejection genes were identified bioinformatically. Western blot, immunofluorescence, and flow cytometry were utilized to measure rejection-related protein levels and T cell surface markers in thymic organoids to determine T cell inducement and immunomodulation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In vitro, TECs, TMCs, and HSCs created thymic aggregates, which became thymic organoids after in vivo transplantation and produced CD8⁺ and CD4⁺ Tregs. Bioinformatics showed high correlations between transplanted rejection and IFNG, IL2RG, FCGR3A, and ICAM1 genes. Immunofluorescence and Western blot showed increased protein expression of IFNG, IL2RG, FCGR3A (immunomodulation biomarker), and decreased protein expression of CK8, CK14, and ICAM1 (TEC biomarker) in thymic organoids.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Thymic organoids heterotopically implanted in vivo can promote heterologous HSC-derived T cell development.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70229","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888187","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}