Translational Research最新文献

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Caspase-12 exhibits non-redundant functions in response to endoplasmic reticulum stress to promote GSDMD-mediated NETosis, leading to thoracic aortic dissection

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-02-25 DOI: 10.1016/j.trsl.2025.02.005

Hanchuan Chen , Kun Yang , Shumin Zhang , Gulinazi Yesitayi , Yunzhi Ling , Rifeng Gao , Yang Lyu , Wei Wei , Jiaran Shi , Yulin Li , Xiang Ma , Pingjin Gao , Junbo Ge , Aijun Sun

Background

Thoracic aortic dissection (TAD) is a highly lethal condition that is characterized by inflammatory cell infiltration. Recent evidence has indicated that Gasdermin D (GSDMD) plays an important role in vascular inflammation and degeneration. However, its effects on neutrophil extracellular trap formation and release (NETosis) during TAD remain unknown.

Methods

A TAD mouse model was generated using four-week-old male neutrophil-specific GSDMD-knockout mice (GSDMD^F/F; Elane^Cre) and dimethyl fumarate (DMF)-treated C57BL/6J mice by administering β-aminopropionitrile monofumarate (BAPN; 1 g/kg/day) in their drinking water for 4 weeks. Immunoprecipitation and immunofluorescence assays were performed to examine the role of the endoplasmic reticulum (ER) and its associated protein, caspase-12, in GSDMD-induced NETosis.

Results

GSDMD was elevated and co-localized primarily in neutrophils in the aortic tissues of patients with TAD and mice with BAPN-induced TAD. This was accompanied by increased NETosis. Neutrophil-specific GSDMD knockout and the NETosis inhibitor, GSK484, mitigated TAD development in mice. However, GSK484 did not provide additional therapeutic effects against TAD in the neutrophil-specific, GSDMD knockout mice. Mechanistically, ER stress promoted GSDMD cleavage by caspase-4/11, thereby inducing NETosis. Furthermore, caspase-12 exhibited non-redundant functions in the cleavage of GSDMD by caspase-4/11. The GSDMD inhibitor, DMF, partially prevented TAD development.

Conclusions

The ER stress/GSDMD/NETosis signaling pathway provides a potential therapeutic target for the prevention and treatment of TAD.

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引用次数: 0

Effects of senotherapeutics on gut microbiome dysbiosis and intestinal inflammation in Crohn's disease: A pilot study

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-02-20 DOI: 10.1016/j.trsl.2025.02.004

Nannapat Sangfuang , Laura E. McCoubrey , Atheer Awad , Massimo Marzorati , Jonas Ghyselinck , Lynn Verstrepen , Julie De Munck , Jelle De Medts , Simon Gaisford , Abdul W. Basit

Inflammatory Bowel Disease (IBD) is characterized by chronic inflammation in the gastrointestinal tract, and is usually accompanied by dysbiosis in the gut microbiome, a factor that contributes to disease progression. Excessive production of reactive oxygen species (ROS) because of gut microbiome dysbiosis—one of the hallmark features of IBD—promotes chronic inflammation and facilitates the transformation of normal cells into senescent cells. Cellular senescence is associated with the development of various chronic and age-related diseases. We hypothesise that senolytic agents, specifically dasatinib (D) and quercetin (Q), could have a beneficial effect on both the gut microbiome and intestinal cells in IBD. The modulatory effects of a combination of D + Q was assessed in the M-SHIME model with faecal microbiota sourced from Crohn's disease patients. D + Q significantly modulated butyrate and lactate levels in the samples from specific patients. In addition, metabolomic analysis showed that D + Q positively impacted the abundance of anti-inflammatory bacteria while also significantly reducing the several species of pathogenic bacteria. Findings from a Caco-2 cell/THP1 co-culture model of IBD demonstrated that D + Q exerted strong immunomodulatory effects on the gut epithelium, evidenced by reduced NF-kB activity, and lower levels of the pro-inflammatory markers TNF-α, CXCL-10, and MCP-1. Furthermore, D + Q induced the secretion of anti-inflammatory cytokines, including IL-6 and IL-10. However, it should be noted that D + Q also led to the secretion of the pro-inflammatory cytokines IL-8. These findings suggest that D + Q could offer a novel therapeutic approach for advanced IBD management by modulating both the gut microbiome and inflammatory pathways. The results support the potential repurposing of senotherapeutic agents as a strategy for addressing the chronic inflammation central to IBD pathogenesis

{"title":"Effects of senotherapeutics on gut microbiome dysbiosis and intestinal inflammation in Crohn's disease: A pilot study","authors":"Nannapat Sangfuang , Laura E. McCoubrey , Atheer Awad , Massimo Marzorati , Jonas Ghyselinck , Lynn Verstrepen , Julie De Munck , Jelle De Medts , Simon Gaisford , Abdul W. Basit","doi":"10.1016/j.trsl.2025.02.004","DOIUrl":"10.1016/j.trsl.2025.02.004","url":null,"abstract":"<div><div>Inflammatory Bowel Disease (IBD) is characterized by chronic inflammation in the gastrointestinal tract, and is usually accompanied by dysbiosis in the gut microbiome, a factor that contributes to disease progression. Excessive production of reactive oxygen species (ROS) because of gut microbiome dysbiosis—one of the hallmark features of IBD—promotes chronic inflammation and facilitates the transformation of normal cells into senescent cells. Cellular senescence is associated with the development of various chronic and age-related diseases. We hypothesise that senolytic agents, specifically dasatinib (D) and quercetin (Q), could have a beneficial effect on both the gut microbiome and intestinal cells in IBD. The modulatory effects of a combination of <em>D</em> + <em>Q</em> was assessed in the M-SHIME model with faecal microbiota sourced from Crohn's disease patients. <em>D</em> + <em>Q</em> significantly modulated butyrate and lactate levels in the samples from specific patients. In addition, metabolomic analysis showed that <em>D</em> + <em>Q</em> positively impacted the abundance of anti-inflammatory bacteria while also significantly reducing the several species of pathogenic bacteria. Findings from a Caco-2 cell/THP1 co-culture model of IBD demonstrated that <em>D</em> + <em>Q</em> exerted strong immunomodulatory effects on the gut epithelium, evidenced by reduced NF-kB activity, and lower levels of the pro-inflammatory markers TNF-α, CXCL-10, and MCP-1. Furthermore, <em>D</em> + <em>Q</em> induced the secretion of anti-inflammatory cytokines, including IL-6 and IL-10. However, it should be noted that <em>D</em> + <em>Q</em> also led to the secretion of the pro-inflammatory cytokines IL-8. These findings suggest that <em>D</em> + <em>Q</em> could offer a novel therapeutic approach for advanced IBD management by modulating both the gut microbiome and inflammatory pathways. The results support the potential repurposing of senotherapeutic agents as a strategy for addressing the chronic inflammation central to IBD pathogenesis</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"278 ","pages":"Pages 36-47"},"PeriodicalIF":6.4,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143474855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Tailored CD4+ lymphocytes expressing human CHAT protein as a novel vasodilator in attenuating RV pressure in PAH animal model

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-02-15 DOI: 10.1016/j.trsl.2025.02.001

Akash Gupta , Nahla Zaghloul , Senthil Kumar Thulasingam , Ian Richard Robbins , Geetanjali Gupta , Jad Bader , Joe GN Garcia , Mohamed Ahmed

ChAT-expressing T cells represent ∼0.01 % of total circulating T lymphocytes in adult wild-type mice. However, we previously reported that systemic infusion of ChAT+ve Jurkat T cells into adult mice elicits vasodilation and instantaneous decline in the mean systolic blood pressure, suggesting potential as a biologic therapeutic to attenuate pathologic increases in pulmonary arterial pressures. We now report that ChAT gene-expressing Jurkat cells dose-dependently decrease right ventricular systolic pressures (RVSP) in hypoxic mice and that transgenic mice with ChAT KO restricted to endothelial cells (KO END/ChAT-/-) exhibit significantly elevated pulmonary arterial pressure and peripheral systemic resistance (compared to WT mice). To rigorously characterize the role of CD4 ChAT+ T cells in regulating pulmonary arterial hypertension (PAH) hemodynamics and molecular signatures, we infused CD4+ ChAT+ve cells (0.5 to 2.0 million cells/animal) into adult PAH mice and noted significant reductions in RVSP within 2-3 min post injection (∼ 50 % reduction). The tailored tail vein injection effect was sustained until the animal was euthanized (30-40 min). Mice KO END/ChAT-/-showed a significant and severe hypoxia-induced PAH phenotype compared to WT adult mice. Tail vein injection of biologically active CD4 ChAT+ve cells into either KO END/ChAT-/-mice with hypoxia-induced PAH or into adult rats with hypoxia/Sugen-induced PAH resulted in significant attenuation of RVP elevations. RNA seq data analysis of human pulmonary endothelial cells (HPAECs) incubated with CD4 ChAT+ve T cells showed significant differential regulation of pathways involved in systemic and pulmonary pressure regulation, NO synthesis/regulation, antioxidant expression, and vasodilation. In conclusion, CD4 ChAT+ve T cells have a unique, vasodilating innate immunity mechanism to augment nitric oxide release and potentially mitigate molecular and genetic pathways involved in PAH pathogenesis.

{"title":"Tailored CD4+ lymphocytes expressing human CHAT protein as a novel vasodilator in attenuating RV pressure in PAH animal model","authors":"Akash Gupta , Nahla Zaghloul , Senthil Kumar Thulasingam , Ian Richard Robbins , Geetanjali Gupta , Jad Bader , Joe GN Garcia , Mohamed Ahmed","doi":"10.1016/j.trsl.2025.02.001","DOIUrl":"10.1016/j.trsl.2025.02.001","url":null,"abstract":"<div><div>ChAT-expressing T cells represent ∼0.01 % of total circulating T lymphocytes in adult wild-type mice. However, we previously reported that systemic infusion of ChAT+ve Jurkat T cells into adult mice elicits vasodilation and instantaneous decline in the mean systolic blood pressure, suggesting potential as a biologic therapeutic to attenuate pathologic increases in pulmonary arterial pressures. We now report that ChAT gene-expressing Jurkat cells dose-dependently decrease right ventricular systolic pressures (RVSP) in hypoxic mice and that transgenic mice with ChAT KO restricted to endothelial cells (KO END/ChAT-/-) exhibit significantly elevated pulmonary arterial pressure and peripheral systemic resistance (compared to WT mice). To rigorously characterize the role of CD4 ChAT+ T cells in regulating pulmonary arterial hypertension (PAH) hemodynamics and molecular signatures, we infused CD4+ ChAT+ve cells (0.5 to 2.0 million cells/animal) into adult PAH mice and noted significant reductions in RVSP within 2-3 min post injection (∼ 50 % reduction). The tailored tail vein injection effect was sustained until the animal was euthanized (30-40 min). Mice KO END/ChAT-/-showed a significant and severe hypoxia-induced PAH phenotype compared to WT adult mice. Tail vein injection of biologically active CD4 ChAT+ve cells into either KO END/ChAT-/-mice with hypoxia-induced PAH or into adult rats with hypoxia/Sugen-induced PAH resulted in significant attenuation of RVP elevations. RNA seq data analysis of human pulmonary endothelial cells (HPAECs) incubated with CD4 ChAT+ve T cells showed significant differential regulation of pathways involved in systemic and pulmonary pressure regulation, NO synthesis/regulation, antioxidant expression, and vasodilation. In conclusion, CD4 ChAT+ve T cells have a unique, vasodilating innate immunity mechanism to augment nitric oxide release and potentially mitigate molecular and genetic pathways involved in PAH pathogenesis.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"278 ","pages":"Pages 22-35"},"PeriodicalIF":6.4,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143443109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Macrophage-driven inflammation in acute kidney injury: Therapeutic opportunities and challenges

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-02-13 DOI: 10.1016/j.trsl.2025.02.003

Ya-Fan Mu , Zi-Hui Mao , Shao-Kang Pan , Dong-Wei Liu , Zhang-Suo Liu , Peng Wu , Zhong-Xiuzi Gao

Acute kidney injury (AKI) is increasingly being recognized as a systemic disorder associated with significant morbidity and mortality. AKI manifests with extensive cellular damage, necrosis, and an intense inflammatory response, often leading to late-stage interstitial fibrosis. Although the mechanisms underlying renal injury and repair remain poorly understood, macrophages (pivotal inflammatory cells) play central roles in AKI. They undergo polarization into pro-inflammatory and anti-inflammatory phenotypes, contributing dynamically to both the injury and repair processes while maintaining homeostasis. Macrophages modulate microenvironmental inflammation by releasing extracellular vesicles (EVs) containing pro- or anti-inflammatory signaling molecules, thereby influencing the regulation of tissue injury. The injured tissue cells release EVs and activate local macrophages to initiate these responses. Our bibliometric analysis indicated that a shift has occurred in AKI macrophage research towards therapeutic strategies and clinical translation, focusing on macrophage-targeted therapies, including exosomes and nanoparticles. This review highlights the roles and mechanisms of macrophage activation, phenotypic polarization, and trans-differentiation in AKI and discusses macrophage-based approaches for AKI prevention and treatment. Understanding the involvement of macrophages in AKI contributes to the comprehension of related immune mechanisms and lays the groundwork for novel diagnostic and therapeutic avenues.

{"title":"Macrophage-driven inflammation in acute kidney injury: Therapeutic opportunities and challenges","authors":"Ya-Fan Mu , Zi-Hui Mao , Shao-Kang Pan , Dong-Wei Liu , Zhang-Suo Liu , Peng Wu , Zhong-Xiuzi Gao","doi":"10.1016/j.trsl.2025.02.003","DOIUrl":"10.1016/j.trsl.2025.02.003","url":null,"abstract":"<div><div>Acute kidney injury (AKI) is increasingly being recognized as a systemic disorder associated with significant morbidity and mortality. AKI manifests with extensive cellular damage, necrosis, and an intense inflammatory response, often leading to late-stage interstitial fibrosis. Although the mechanisms underlying renal injury and repair remain poorly understood, macrophages (pivotal inflammatory cells) play central roles in AKI. They undergo polarization into pro-inflammatory and anti-inflammatory phenotypes, contributing dynamically to both the injury and repair processes while maintaining homeostasis. Macrophages modulate microenvironmental inflammation by releasing extracellular vesicles (EVs) containing pro- or anti-inflammatory signaling molecules, thereby influencing the regulation of tissue injury. The injured tissue cells release EVs and activate local macrophages to initiate these responses. Our bibliometric analysis indicated that a shift has occurred in AKI macrophage research towards therapeutic strategies and clinical translation, focusing on macrophage-targeted therapies, including exosomes and nanoparticles. This review highlights the roles and mechanisms of macrophage activation, phenotypic polarization, and trans-differentiation in AKI and discusses macrophage-based approaches for AKI prevention and treatment. Understanding the involvement of macrophages in AKI contributes to the comprehension of related immune mechanisms and lays the groundwork for novel diagnostic and therapeutic avenues.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"278 ","pages":"Pages 1-9"},"PeriodicalIF":6.4,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143418852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Multi-Omics Analysis Links Mitochondrial-Related Genes to Idiopathic Pulmonary Fibrosis and In Vivo Transcriptome Validation

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-02-12 DOI: 10.1016/j.trsl.2025.02.002

Xiaoxia Li , Qiaojing Lin , Bingyue Guan , Minghuan Yang , Xingxin Huang , Lianhuang Li , Chun Chen , Jinsheng Hong , Mingwei Zhang

Mitochondrial dysfunction is closely associated with idiopathic pulmonary fibrosis (IPF). However, the causal association between mitochondria-related genes and IPF remains to be determined. We obtained gene expression, protein abundance, and methylation quantitative trait locus data for mitochondria-related genes from previous studies. Genome-wide association study data for patients with IPF were obtained from the FinnGen study. A two-sample Mendelian randomisation analysis was conducted to assess the association between mitochondria-related genes and IPF. Furthermore, we conducted validation of expression differences utilizing transcriptome data derived from the BLM-induced pulmonary fibrosis mouse model (n=15). Concurrently, multiphoton imaging was utilized to quantify collagen contents and structural assessment. The direction of causality was verified using the Steiger test, and colocalisation analysis was used to better validate causality. Single-cell data were used to explore the localisation and expression of positive genes across different cell types. The study identified significant associations between mitochondria-related genes and IPF, with POLG and NDUFB10 classified as Grade 1; LYRM4, NBR1, and ACSF3 as Grade 2; MCL1, GFER, MFN2, IVD, and SLC25A35 as Grade 3; and METAP1D and MTX1 as Grade 4. Single-cell analysis showed elevated expression of NBR1, MCL1, and MTX1 in pulmonary myofibroblasts of IPF. This study elucidated the causal effects of mitochondria-related genes on IPF, underscoring their significance in pathogenesis. These findings contribute to an improved understanding of the mechanisms underlying IPF, offering new potential therapeutic targets for interventions.

{"title":"Multi-Omics Analysis Links Mitochondrial-Related Genes to Idiopathic Pulmonary Fibrosis and In Vivo Transcriptome Validation","authors":"Xiaoxia Li , Qiaojing Lin , Bingyue Guan , Minghuan Yang , Xingxin Huang , Lianhuang Li , Chun Chen , Jinsheng Hong , Mingwei Zhang","doi":"10.1016/j.trsl.2025.02.002","DOIUrl":"10.1016/j.trsl.2025.02.002","url":null,"abstract":"<div><div>Mitochondrial dysfunction is closely associated with idiopathic pulmonary fibrosis (IPF). However, the causal association between mitochondria-related genes and IPF remains to be determined. We obtained gene expression, protein abundance, and methylation quantitative trait locus data for mitochondria-related genes from previous studies. Genome-wide association study data for patients with IPF were obtained from the FinnGen study. A two-sample Mendelian randomisation analysis was conducted to assess the association between mitochondria-related genes and IPF. Furthermore, we conducted validation of expression differences utilizing transcriptome data derived from the BLM-induced pulmonary fibrosis mouse model (n=15). Concurrently, multiphoton imaging was utilized to quantify collagen contents and structural assessment. The direction of causality was verified using the Steiger test, and colocalisation analysis was used to better validate causality. Single-cell data were used to explore the localisation and expression of positive genes across different cell types. The study identified significant associations between mitochondria-related genes and IPF, with <em>POLG</em> and <em>NDUFB10</em> classified as Grade 1; <em>LYRM4, NBR1</em>, and <em>ACSF3</em> as Grade 2; <em>MCL1, GFER, MFN2, IVD</em>, and <em>SLC25A35</em> as Grade 3; and <em>METAP1D</em> and <em>MTX1</em> as Grade 4. Single-cell analysis showed elevated expression of <em>NBR1, MCL1</em>, and <em>MTX1</em> in pulmonary myofibroblasts of IPF. This study elucidated the causal effects of mitochondria-related genes on IPF, underscoring their significance in pathogenesis. These findings contribute to an improved understanding of the mechanisms underlying IPF, offering new potential therapeutic targets for interventions.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"278 ","pages":"Pages 10-21"},"PeriodicalIF":6.4,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143426815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Author Guidelines

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-02-11 DOI: 10.1016/S1931-5244(25)00017-9

引用次数: 0

Information for Readers

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-02-11 DOI: 10.1016/S1931-5244(25)00018-0

引用次数: 0

Editorial Advisory Board

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-02-11 DOI: 10.1016/S1931-5244(25)00016-7

引用次数: 0

Corrigendum to “Early vascular aging in chronic kidney disease: focus on microvascular maintenance, senescence signature and potential therapeutics” [Translational Research 275 (2025) 32–47] “慢性肾脏疾病的早期血管衰老：关注微血管维持、衰老特征和潜在治疗方法”[Translational Research] 275(2025) 32-47]。

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-02-01 DOI: 10.1016/j.trsl.2024.12.003

Samsul Arefin , Neja Mudrovcic , Sam Hobson , Federico Pietrocola , Thomas Ebert , Liam J. Ward , Anna Witasp , Leah Hernandez , Lars Wennberg , Torbjörn Lundgren , Julia Steinmetz-Späh , Karin Larsson , Anders Thorell , Stefania Bruno , Marita Marengo , Vincenzo Cantaluppi , Peter Stenvinkel , Karolina Kublickiene

引用次数: 0

Infectious agents in the pathogenesis of autoimmune rheumatic diseases 自身免疫性风湿病发病机制中的传染因子。

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-02-01 DOI: 10.1016/j.trsl.2024.12.004

Aleksandra Korzeniowska, Ewa Bryl

Autoimmune rheumatic diseases (AIRDs) are diseases with complex outset and courses, in which both genetic and environmental factors participate. Many environmental factors can be committed to AIRDs outset and development. The most popular of them, with confirmed impact, are smoking, age, gender, and microorganisms. In light of recent research an assumption about the importance of various microorganisms in the pathogenesis of AIRDs is growing in popularity.

The human immune system has various protective mechanisms against infectious antigens which in normal cases let organism manage potential infection faster and more effectively. Unfortunately in some situations, specific errors in those mechanisms can cause an autoreactive response despite mitigation of infection. Viruses including EBV, CMV, and even SARS-CoV2 can cause these errors. This in combination with genetic factors can lead to rheumatic disease development.

This research aims to provide a brief review of the role of viruses in the outset and development of AIRDs.

自身免疫性风湿病（AIRDs）是一种发病和病程复杂的疾病，遗传和环境因素都参与其中。许多环境因素可以对aird的开始和发展作出承诺。其中最受欢迎的是吸烟、年龄、性别和微生物。根据最近的研究，关于各种微生物在AIRDs发病机制中的重要性的假设越来越受欢迎。人体免疫系统对感染性抗原有多种保护机制，在正常情况下，这些机制使生物体更快、更有效地控制潜在的感染。不幸的是，在某些情况下，这些机制中的特定错误可能导致自身反应性反应，尽管感染减轻了。包括EBV、CMV甚至SARS-CoV2在内的病毒都可能导致这些错误。这与遗传因素相结合可导致风湿病的发展。本研究旨在简要回顾病毒在AIRDs发病和发展中的作用。

引用次数: 0

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