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Interferon regulatory factor 4-releasing 3D-printed scaffolds enhance spinal cord repair by modulating macrophage polarization 认领 引用 被引量：1
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作者 Jianhao Wang Jiawei Du +5 位作者 Tuo Fang Di Zhang Yigang Lv Zhongju Shi Hengxing Zhou Shiqing Feng 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第8期3706-3716,共11页
Three-dimensional(3D)-printed hydrogel scaffolds are widely used in spinal cord injury repair,with gelatin methacrylate being particularly favored owing to its excellent biocompatibility.However,traditional scaffolds ... Three-dimensional(3D)-printed hydrogel scaffolds are widely used in spinal cord injury repair,with gelatin methacrylate being particularly favored owing to its excellent biocompatibility.However,traditional scaffolds have a small contact area with tissues and lack the ability to regulate the inflammatory microenvironment.Therefore,there is a need to develop smart scaffolds with drug delivery and immune regulation functions.In this study,a 3D-printed gelatin methacrylate scaffold was developed to deliver interferon regulatory factor 4 in a targeted and sustained manner.The scaffold showed good mechanical properties,biocompatibility,and sustained interferon regulatory factor 4 release.The sustained-release interferon regulatory factor 4 competitively bound to myeloid differentiation factor 88 to inhibit the pro-inflammatory effects of interferon regulatory factor 5,and activated the signal transducer and activator of transcription 6 pathway to promote M2 macrophage polarization,thereby facilitating neural regeneration and recovery of spinal cord function.This indicates that the constructed interferon regulatory factor 4-loaded 3D-printed methyl acrylate-modified gelatin scaffold can regulate macrophage polarization through the interferon regulatory factor 4/5 axis,improve the inflammatory microenvironment after spinal cord injury,and thus provide a new target for promoting neural regeneration. 展开更多
关键词 3D-printed scaffold inflammatory microenvironment interferon regulatory factor 4 JAK1/STAT6 signaling pathway macrophage polarization microglia nerve regeneration spinal cord injury
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Interferon regulatory factor 1 enhances T cell differentiation in patients with myasthenia gravis 认领 引用 被引量：1
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作者 Yuebei Luo Yijun Ren +3 位作者 Zeyi Wen Zhaohui Luo Huan Yang Liqun Xu 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第7期3267-3280,共14页
Interferon regulatory factor 1 is involved in many autoimmune conditions and is increased in patients with myasthenia gravis.However,its function in myasthenia gravis remains unclear.Herein,we explored the function of... Interferon regulatory factor 1 is involved in many autoimmune conditions and is increased in patients with myasthenia gravis.However,its function in myasthenia gravis remains unclear.Herein,we explored the function of interferon regulatory factor 1 in myasthenia gravis,with an aim to understand the underlying mechanisms.Patients with myasthenia gravis who had acetylcholine receptor antibodies were included in the study.Peripheral blood lymphocytes were extracted from the included patients,and B lymphocyte subsets were isolated.Next,T and B cells from peripheral blood were co-cultured to explore the interferon regulatory factor 1-related mechanisms in myasthenia gravis.Chromatin immunoprecipitation experiments confirmed an interaction between interferon regulatory factor 1 and the CD180 promoter region.Dual-luciferase reporter gene confirmed the transcriptional activity of interferon regulatory factor 1 on CD180 promoter.In vitro results further indicated that interferon regulatory factor 1 promoted B cell activation and T cell differentiation via the inhibition of CD180.Interferon regulatory factor 1 recruited histone deacetylase 1 to inhibit CD180 transcription.Additionally,histone deacetylase 1 promoted B cell activation and T cell differentiation.Finally,in vitro experiments demonstrated that CD180 inhibited B cell activation and T cell differentiation by inhibiting the Toll-like receptor 4/mitogen-activated protein kinasesuclear factor-kappa B pathway.Collectively,our results suggest that interferon regulatory factor 1 enhances T cell differentiation by recruiting histone deacetylase 1 to block B cell CD180 transcription in myasthenia gravis via the Toll-like receptor 4/mitogen-activated protein kinasesuclear factor-kappa B pathway.Together,these findings indicate the important role of interferon regulatory factor 1 in myasthenia gravis and suggest its molecular mechanisms.They also provide new ideas and targets for diagnosing and treating myasthenia gravis,which will be both scientifically and clinically valuable. 展开更多
关键词 autoimmune condition B cell CD180 histone deacetylase 1 interferon regulatory factor 1 mitogen-activated protein kinase myasthenia gravis nuclear factor-kappa B T cell Toll-like receptor 4
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Integrated transcriptomics and metabolomics reveal neutrophil extracellular trap associated with interferon treatment for chronic hepatitis B 认领 引用
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作者 Xiang-Yang Ye Xiong-Zhi He +6 位作者 Zhen-Ting Hu Feng-Feng Zheng Xiao-Gang Huang Xue-Mei Xie Fei-Hua Chen Han-Bing Ou Rong-Xian Qiu 《World Journal of Hepatology》 2026年第4期172-189,共18页
BACKGROUND Chronic hepatitis B(CHB)is a significant global health issue,and interferon(IFN)is one of the main first-line therapies for CHB.AIM To investigate the altered transcriptome,metabolites,and their correlation... BACKGROUND Chronic hepatitis B(CHB)is a significant global health issue,and interferon(IFN)is one of the main first-line therapies for CHB.AIM To investigate the altered transcriptome,metabolites,and their correlations,as well as the effects and mechanisms of IFN treatment for CHB.METHODS The patients received peginterferon alfa-2b at a dose of 180μg for 0,1,3,and 6 months and serum samples were collected for clinical biological assays,transcriptomics,and metabolomics analyses.RESULTS The results showed that IFN-related immune pathways and neutrophil extracellular traps(NETs)were the most significantly altered pathways following IFN treatment.Correlation analysis revealed a strong link between immune system-related genes in the transcriptome and dipeptides in the metabolome during IFN-αtreatment.Notably,core components of NETs,including histones H2A clustered histone 14,H2B clustered histone 5,H3 clustered histone 1,and H4 clustered histone 4,were significantly increased after IFN treatment.The positively charged histones may bind to the negatively charged viral envelope,potentially enhancing the antiviral effect.CONCLUSION Integrated non-targeted transcriptomic and metabolomic analyses to CHB patients undergoing IFN-αtreatment revealed that IFN-related immune pathways and NETs were the most significantly affected pathways during IFN treatment.These findings provide a deeper understanding of the role of NETs and dipeptides in the antiviral response to IFN treatment for CHB. 展开更多
关键词 Interferon Neutrophil extracellular trap Chronic hepatitis B Hepatitis B virus Transcriptomic and metabolomic
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Baseline hepatitis B surface antigen and cirrhosis predict extended interferon therapy in chronic hepatitis B:A retrospective study 认领 引用
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作者 Fei Yan Xiu-Lan Xue +20 位作者 Ying Guo Qi-Ran Zhang Rui-Rui You Jia Shang Xiao-Ping Wu Jia-Wei Geng Xiao-Hong Gao Qing Ye Jing Liang Xiao-Yan Wang Jian-Yong Zeng Jing Chen Yi-Cheng Lin Xin-Yu Chen Qin Du Wei-Li Yin Lei Liu Fang Wang Bai-Guo Xu Wen-Hong Zhang Hui-Ling Xiang 《World Journal of Gastroenterology》 SCIE CAS 2026年第12期62-76,共15页
BACKGROUND Chronic hepatitis B(CHB)is a major global health burden,with China being the most affected.Achieving a clinical cure,defined as hepatitis B surface antigen(HBsAg)clearance,is the ideal treatment endpoint.Wh... BACKGROUND Chronic hepatitis B(CHB)is a major global health burden,with China being the most affected.Achieving a clinical cure,defined as hepatitis B surface antigen(HBsAg)clearance,is the ideal treatment endpoint.While a 48-week interferon course is standard,extended therapy may improve HBsAg clearance rates.However,there exists a notable gap in predictive modeling studies concerning extended treatment courses(≥48 weeks).AIM To develop a predictive model for identifying patients who require extended interferon therapy(≥48 weeks)for HBsAg clearance.METHODS This multicenter retrospective study included CHB patients,including those with compensated cirrhosis,who achieved HBsAg clearance(HBsAg<0.05 IU/mL)following treatment with pegylated interferon alpha-2b,either alone or in combination with nucleoside analogs.After propensity score matching,we employed least absolute shrinkage and selection operator(LASSO)regression and multivariate regression to identify independent predictors.RESULTS A total of 688 eligible patients with CHB were enrolled in this study.After propensity score matching at a 1:1 ratio,375 patients remained,including 196 in the training cohort.Among the training cohort,36(18.37%)were classified in the extended course(≥48 weeks)and 160(81.63%)in the regular course(<48 weeks).LASSO and multivariate regression analyses identified baseline HBsAg and cirrhosis as significant risk factors for extended interferon therapy.The model demonstrated strong discriminatory ability,with the area under the curve of 0.83[95%confidence interval(CI):0.76-0.91]for the training cohort and 0.81(95%CI:0.71-0.90)for the externally validated cohort.The model’s predictive efficacy was not influenced by subgroup characteristics.CONCLUSION This study successfully constructed and validated a prediction model based on baseline HBsAg and cirrhosis to identify potential populations that may benefit from extended interferon therapy(≥48 weeks). 展开更多
关键词 Chronic hepatitis B Clinical cure Extended course of interferon Hepatitis B surface antigen Prediction model
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Two orthobunyaviruses:OYAV and EBIV co-opt the AhR-CYP1A1 axis to suppress type I interferon responses 认领 引用
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作者 Qianyun Hu Fei Wang +4 位作者 Xiaoyu Wang Xiaokui Li Zhiming Yuan Maohua Zhong Han Xia 《Virologica Sinica》 SCIE CAS CSCD 2026年第2期329-342,共14页
The type I interferon(IFN-I)system serves as a frontline defense against viral infection,yet how orthobunyaviruses counteract this pathway remains poorly defined.Here,we identify cytochrome P4501A1(CYP1A1)as a crucial... The type I interferon(IFN-I)system serves as a frontline defense against viral infection,yet how orthobunyaviruses counteract this pathway remains poorly defined.Here,we identify cytochrome P4501A1(CYP1A1)as a crucial host factor promoting infection by two emerging orthobunyaviruses-Oya virus(OYAV)and Ebinur Lake virus(EBIV).Transcriptomic and functional analyses demonstrate that CYP1A1 overexpression enhances viral RNA synthesis,whereas its CRISPR-Cas9mediated knockout attenuates infection.Mechanistically,OYAV and EBIV activate the aryl hydrocarbon receptor(AhR),driving its nuclear translocation and subsequent upregulation of CYP1A1.Deficiency of CYP1A1 potentiates IFN-βproduction and interferon-stimulated gene(ISG)expression,while its overexpression suppressed antiviral signaling,revealing an immunomodulatory role that is distinct from its canonical metabolic function.Collectively,this work defines the AhR-CYP1A1 axis as a conserved immune-evasion module exploited by emerging orthobunyaviruses and highlights the innate immune pathway as a potential therapeutic target against these emerging threats. 展开更多
关键词 Orthobunyavirus Cytochrome P4501A1(CYP1A1) Type I interferon(IFN-I) Aryl hydrocarbon receptor(AhR) Immune evasion
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Effects of pegylated interferon on T cell receptor fingerprints in chronic hepatitis B patients with/without surface antigen clearance 认领 引用
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作者 Kun-Yan Hao Lei Tang +4 位作者 Guo-Bing Chen Wei Guo Zhan-Hui Wang Li-Peng Mao Yue-Cheng Yu 《World Journal of Hepatology》 2026年第7期73-84,共12页
BACKGROUND Chronic hepatitis B(CHB)remains a critical global health challenge,with few patients achieving spontaneous clearance of hepatitis B surface antigen(HBsAg),which is a key indicator of functional cure.T cell ... BACKGROUND Chronic hepatitis B(CHB)remains a critical global health challenge,with few patients achieving spontaneous clearance of hepatitis B surface antigen(HBsAg),which is a key indicator of functional cure.T cell plays an important role in HBsAg clearance.AIM To compare T cell receptor(TCR)fingerprints between patients with or without HBsAg clearance after pegylated interferon alpha-2b(PegIFNα-2b)added on nucleos(t)ide analogues(NAs).METHODS In this observational study,peripheral blood mononuclear cells(PBMCs)were isolated from six comparable CHB patients who achieved HBsAg clearance(Group-C)or not(Group-NC)after 48 weeks of PegIFNα-2b added to NA therapy.Patients in Group-C and Group-NC had comparable age,gender,baseline hepatitis B virus(HBV)DNA,HBsAg,hepatitis B envelop antigen(HBeAg),total bilirubin,alanine aminotransferase(ALT)and cirrhosis status.All patients had received at least one year of NA before PegIFNα-2b therapy.TCR repertoire profiles(fingerprints)were screened and compared by RNA sequencing and bioinformation analysis between the two groups.RESULTS Six male patients without cirrhosis were enrolled in this study,with three patients in each group.200 ng of RNA from each PBMC sample was extracted for standard RNA sequencing for construction of a complementary DNA library.Baseline levels of HBsAg,HBeAg,HBV DNA(0.05).It was found that compared to Group-NC,Group-C had significantly higher TCR diversity in bothαandβchain,including more unique clonotypes(P=0.017,P=0.038 respectively),more repertoire overlap(P=0.002,P=0.002 respectively),a broader complementarity-determining region3 length distribution,and higher Chao1 index(P=0.016,P=0.048 respectively).CONCLUSION Patients with HBsAg clearance had a more diverse and robust T cell response,which may correlate with HBsAg clearance status.These immune signatures may serve as potential reference indicators for PegIFNα-2b treatment response in CHB patients. 展开更多
关键词 Hepatitis B surface antigen clearance Pegylated interferonα-2b T cell receptor diversity Complementaritydetermining region 3 RNA sequencing Fingerprints
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Interferon-gamma signaling pathway:Modulation of key genes in the progression of glioblastoma 认领 引用
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作者 Enrique Oropeza-Martínez Eva G Palacios Serrato +4 位作者 Sayra X Zamora-Salas Norma A Lira-Rodríguez Sianka’an HZ López-Mignon Maximo B Martinez-Benitez Angeles C Tecalco-Cruz 《World Journal of Biological Chemistry》 2025年第4期52-64,共13页
The canonical signaling of interferon gamma(IFN-γ)through the Janus kinase 1 and 2–signal transducer and activator of transcription 1(STAT1)axis leads to the expression of several interferon-stimulated genes(ISGs),w... The canonical signaling of interferon gamma(IFN-γ)through the Janus kinase 1 and 2–signal transducer and activator of transcription 1(STAT1)axis leads to the expression of several interferon-stimulated genes(ISGs),which have diverse effects depending on the cellular context.In glioblastoma,a highly aggressive primary brain tumor in adults,elements of IFN-γcanonical signaling are deregulated,resulting in the overexpression of STAT1-target ISGs associated with tumor progression.This mini-review highlights key ISGs,including STAT1,interferon regulatory factor 1,programmed death-ligand 1,indoleamine 2,3-dioxygenase 1,and interferon-stimulated gene 15,involved in the pathology of glioblastoma.These genes may serve as valuable biomarkers and have therapeutic potential for targeting IFN-γsignaling in this malignancy. 展开更多
关键词 Glioblastoma Interferon gamma Janus kinases Interferon-stimulated genes Signal transducer and activator of transcription 1 Interferon regulatory factor 1 B7-H1 antigen Indoleamine-2,3-dioxygenase Interferon-stimulated gene 15 Signal transduction
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The cGAS-STING-interferon regulatory factor 7 pathway regulates neuroinflammation in Parkinson's disease 认领 引用 被引量：3
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作者 Shengyang Zhou Ting Li +8 位作者 Wei Zhang Jian Wu Hui Hong Wei Quan Xinyu Qiao Chun Cui Chenmeng Qiao Weijiang Zhao Yanqin Shen 《Neural Regeneration Research》 SCIE CAS CSCD 2025年第8期2361-2372,共12页
Interferon regulatory factor 7 plays a crucial role in the innate immune response.However,whether interferon regulatory factor 7-mediated signaling contributes to Parkinson's disease remains unknown.Here we report... Interferon regulatory factor 7 plays a crucial role in the innate immune response.However,whether interferon regulatory factor 7-mediated signaling contributes to Parkinson's disease remains unknown.Here we report that interferon regulatory factor 7 is markedly up-regulated in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse model of Parkinson's disease and co-localizes with microglial cells.Both the selective cyclic guanosine monophosphate adenosine monophosphate synthase inhibitor RU.521 and the stimulator of interferon genes inhibitor H151 effectively suppressed interferon regulatory factor 7 activation in BV2 microglia exposed to 1-methyl-4-phenylpyridinium and inhibited transformation of mouse BV2 microglia into the neurotoxic M1 phenotype.In addition,si RNA-mediated knockdown of interferon regulatory factor 7 expression in BV2 microglia reduced the expression of inducible nitric oxide synthase,tumor necrosis factorα,CD16,CD32,and CD86 and increased the expression of the anti-inflammatory markers ARG1 and YM1.Taken together,our findings indicate that the cyclic guanosine monophosphate adenosine monophosphate synthase-stimulator of interferon genes-interferon regulatory factor 7 pathway plays a crucial role in the pathogenesis of Parkinson's disease. 展开更多
关键词 cyclic guanosine monophosphate adenosine monophosphate synthase H151 interferon regulatory factor 7 M1 phenotype neurodegenerative disease neuroinflammation Parkinson’s disease RU521 STING type I interferon
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Bidirectional regulation of the cyclic guanosine monophosphateadenosine monophosphate synthase-stimulator of interferon gene pathway and its impact on hepatocellular carcinoma 认领 引用 被引量：1
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作者 Ai-Yu Nie Zhong-Hui Xiao +4 位作者 Jia-Li Deng Na Li Li-Yuan Hao Sheng-Hao Li Xiao-Yu Hu 《World Journal of Gastrointestinal Oncology》 SCIE 2025年第2期246-261,共16页
BACKGROUND Hepatocellular carcinoma(HCC)ranks as the fourth leading cause of cancerrelated deaths in China,and the treatment options are limited.The cyclic guanosine monophosphate-adenosine monophosphate synthase(cGAS... BACKGROUND Hepatocellular carcinoma(HCC)ranks as the fourth leading cause of cancerrelated deaths in China,and the treatment options are limited.The cyclic guanosine monophosphate-adenosine monophosphate synthase(cGAS)activates the stimulator of interferon gene(STING)signaling pathway as a crucial immune response pathway in the cytoplasm,which detects cytoplasmic DNA to regulate innate and adaptive immune responses.As a potential therapeutic target,cGASSTING pathway markedly inhibits tumor cell proliferation and metastasis,with its activation being particularly relevant in HCC.However,prolonged pathway activation may lead to an immunosuppressive tumor microenvironment,which fostering the invasion or metastasis of liver tumor cells.AIM To investigate the dual-regulation mechanism of cGAS-STING in HCC.METHODS This review was conducted according to the PRISMA guidelines.The study conducted a comprehensive search for articles related to HCC on PubMed and Web of Science databases.Through rigorous screening and meticulous analysis of the retrieved literature,the research aimed to summarize and elucidate the impact of the cGAS-STING pathway on HCC tumors.RESULTS All authors collaboratively selected studies for inclusion,extracted data,and the initial search of online databases yielded 1445 studies.After removing duplicates,remaining 964 records were screened.Ultimately,55 articles met the inclusion criteria and were included in this review.CONCLUSION Acute inflammation can have a few inhibitory effects on cancer,while chronic inflammation generally promotes its progression.Extended cGAS-STING pathway activation will result in a suppressive tumor microenvironment. 展开更多
关键词 Hepatocellular carcinoma Cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon gene Interferon genes The metastasis of a tumor Immunology
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Retreatment hepatitis B surface antigen clearance prediction model identifies pegylated interferon alpha candidates in chronic hepatitis B 认领 引用 被引量：1
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作者 Yan-Chao Fu Jun Li +8 位作者 Jia-Yin Wang Yi-Wen Zhang Fei Yan Jing Chen Qin Du Chao Yang Jing Liang Qing Ye Hui-Ling Xiang 《World Journal of Gastroenterology》 SCIE CAS 2025年第44期94-106,共13页
BACKGROUND Chronic hepatitis B(CHB)patients rarely achieve functional cure with initial pegylated interferon alpha-2b(Peg-IFNα-2b)therapy.Validated tools to guide retreatment candidates are lacking.We hypothesized th... BACKGROUND Chronic hepatitis B(CHB)patients rarely achieve functional cure with initial pegylated interferon alpha-2b(Peg-IFNα-2b)therapy.Validated tools to guide retreatment candidates are lacking.We hypothesized that clinical indicators predict hepatitis B surface antigen(HBsAg)clearance during retreatment.AIM To develop a prediction model for HBsAg clearance in Peg-IFNα-2b retreatment.METHODS In this retrospective cohort study,we enrolled 135 CHB/compensated cirrhosis patients receiving Peg-IFNα-2b retreatment after initial non-clearance at Tianjin University Central Hospital(2017-2025).Predictors were identified through univariate Cox,least absolute shrinkage and selection operator,and multivariate Cox regression.Model performance was assessed via receiver operating characteristic analysis and Harrell’s C-index,with risk stratification by X-tile optimization.RESULTS HBsAg clearance rate was 20.74%(28/135).Independent predictors included:Combination nucleos(t)ide analogue(NA)therapy during initial treatment[hazard ratio(HR)=0.276,95%confidence interval(CI):0.092-0.833],baseline HBsAg at retreatment(HR=0.571,95%CI:0.410-0.795),HBsAg decline after initial treatment(HR=2.050,95%CI:1.108-3.793),and treatment interval(HR=1.013/week,95%CI:1.008-1.018).The retreatment HBsAg clearance prediction score(RHCP-S)demonstrated area under the curve of 0.920(95%CI:0.863-0.946),sensitivity of 92.3%,specificity of 79.3%.Clearance rates differed significantly:RHCP-S challenge group(≤74 points):3.45%,RHCP-S probable group(74-110 points):29.63%,RHCP-S dominant group(≥110 points):80.95%(P<0.001).CONCLUSION The overall HBsAg clearance rate with Peg-IFNα-2b retreatment was 20.74%(28/135).The RHCP-S model identifies optimal retreatment candidates(≥110 points)with 80.95%clearance probability,associated with the absence of combination NA therapy during initial treatment,greater initial HBsAg decline,longer intervals,and lower retreatment HBsAg. 展开更多
关键词 Chronic hepatitis B Retreatment Pegylated interferon alpha Hepatitis B surface antigen clearance Prediction model
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Brain endothelial cyclic GMP-AMP synthase(cGAS)-stimulator of interferon genes(STING)signaling pathway in aging and neurodegeneration 认领 引用 被引量：1
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作者 Bryan Sun Lulin Li Jian Luo 《Neural Regeneration Research》 SCIE CAS CSCD 2025年第7期2005-2007,共3页
The cyclic GMP-AMP synthase(cGAS)-stimulator of interferon genes(STING)signaling pathway has emerged as a key mediator of neuroinflammation.While current studies primarily attribute its effects to neurons and glial ce... The cyclic GMP-AMP synthase(cGAS)-stimulator of interferon genes(STING)signaling pathway has emerged as a key mediator of neuroinflammation.While current studies primarily attribute its effects to neurons and glial cells,emerging research suggests that cGAS-STING signaling may play a critical role in cerebral vasculature,particularly in brain endothelial cells.Therefore,studying the role 7of inflammation caused by the cGAS-STING pathway in brain endothelial cells could provide a more comprehensive understanding of neuroinflammatory disease and new avenues for therapeutic interventions.Here,we review the multifaceted role of global cGAS-STING signaling in various neurological and neuroinflammatory diseases and the potential contribution of cGAS-STING in brain endothelial cells. 展开更多
关键词 stimulator interferon inflammation
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Association of interferon regulatory factor 8 dysregulation with dry eye in Sjögren’s syndrome 认领 引用 被引量：1
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作者 Jiao Wang Guang-Hong Chu +4 位作者 Zi-Huan Wang Xiao-Yu Cai Si-Yuan Shi Qi-Ping Qing Qi Zhang 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2025年第8期1456-1463,共8页
AIM:To investigate the expression of interferon regulatory factors(IRFs)in peripheral blood mononuclear cells(PBMCs)of patients with Sjögren’s syndrome-related dry eye(SSDE)and to explore their correlation with ... AIM:To investigate the expression of interferon regulatory factors(IRFs)in peripheral blood mononuclear cells(PBMCs)of patients with Sjögren’s syndrome-related dry eye(SSDE)and to explore their correlation with clinical features,dendritic cell activation,and serological indicators.METHODS:A total of 53 SSDE patients and 62 non-Sjögren’s syndrome dry eye(NSSDE)patients were enrolled.Demographic and clinical data were collected,and comprehensive ophthalmic examinations were performed,including the ocular surface disease index(OSDI)questionnaires,Schirmer I test(SIT),tear break-up time(TBUT),corneal fluorescein staining score(CFS),and in vivo confocal microscopy(IVCM).PBMCs were isolated,and IRFs expression levels were analyzed using Western blotting(WB)and quantitative real-time polymerase chain reaction(qRT-PCR).Serological indicators,including antinuclear antibodies(ANA)and anti-Ro60,anti-Ro52,and anti-La autoantibodies,were detected.Statistical analyses evaluated correlations between IRFs expression and clinical parameters.RESULTS:Compared to NSSDE,the relative mRNA and protein expression of the IRF-8 was significantly upregulated in patients with SSDE(P<0.001),whereas no significant differences were observed in IRF-1,IRF-3,IRF-5,and IRF-7(P=0.12,P=0.10,P=0.66,P=0.96).Correlation analysis revealed that IRF-8 expression was positively associated with CFS and OSDI scores(r=0.57,r=0.38,both P<0.05).Moreover,IRF-8 expression correlated with corneal dendritic cell(DC)density and size,and the number of dendrites(r=0.43,r=0.40,r=0.65,all P<0.05).IRF-8 expression was significantly elevated in patients positive for anti-Ro60,anti-Ro52 and anti-La autoantibodies(P<0.05).CONCLUSION:In SSDE,IRF-8 is upregulated and associated with clinical features,DC activation,and serological indicators.These findings suggest that IRF-8 plays a critical role in SSDE pathogenesis and may serve as a potential therapeutic target for diagnosis and treatment. 展开更多
关键词 interferon regulatory factors Sjögren’s syndrome dry eye
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Role of interferons in diabetic retinopathy 认领 引用 被引量：1
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作者 Bing-Yan Li Wei Tan +4 位作者 Jing-Ling Zou Yan He Shigeo Yoshida Bing Jiang Ye-Di Zhou 《World Journal of Diabetes》 SCIE 2021年第7期939-953,共15页
Diabetic retinopathy(DR)is one of the major causes of visual impairment and irreversible blindness in developed regions.Aside from abnormal angiogenesis,inflammation is the most specific and might be the initiating fa... Diabetic retinopathy(DR)is one of the major causes of visual impairment and irreversible blindness in developed regions.Aside from abnormal angiogenesis,inflammation is the most specific and might be the initiating factor of DR.As a key participant in inflammation,interferon-gamma(IFN-γ)can be detected in different parts of the eye and is responsible for the breakdown of the blood-retina barrier and activation of inflammatory cells and other cytokines,which accelerate neovascularization and neuroglial degeneration.In addition,IFN-γis involved in other vascular complications of diabetes mellitus and angiogenesis-dependent diseases,such as diabetic nephropathy,cerebral microbleeds,and age-related macular degeneration.Traditional treatments,such as anti-vascular endothelial growth factor agents,vitrectomy,and laser photocoagulation therapy,are more effective for angiogenesis and not tolerable for every patient.Many ongoing clinical trials are exploring effective drugs that target inflammation.For instance,IFN-αacts against viruses and angiogenesis and is commonly used to treat malignant tumors.Moreover,IFN-αhas been shown to contribute to alleviating the progression of DR and other ocular diseases.In this review,we emphasize the roles that IFNs play in the pathogenesis of DR and discuss potential clinical applications of IFNs in DR,such as diagnosis,prognosis,and therapeutic treatment. 展开更多
关键词 Interferons Cytokines Diabetic retinopathy Interferon-alpha Interferongamma Inflammation
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Jianpi Yifei Tongluo recipe(健脾益肺通络方剂)attenuates inflammation by promoting the expression of interferon regulatory factor 4 in the rat model of chronic obstructive pulmonary disease 认领 引用
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作者 WANG Wei LONG Qi +1 位作者 FU Ling WU Haiqiao 《Journal of Traditional Chinese Medicine》 SCIE CAS CSCD 2025年第5期1048-1058,共11页
OBJECTIVE:To examine the effects of the Jianpi Yifei Tongluo recipe(健脾益肺通络方剂,JYTR)on chronic obstructive pulmonary disease(COPD)within an animal model and to elucidate its anti-inflammatory mechanisms.METHODS:... OBJECTIVE:To examine the effects of the Jianpi Yifei Tongluo recipe(健脾益肺通络方剂,JYTR)on chronic obstructive pulmonary disease(COPD)within an animal model and to elucidate its anti-inflammatory mechanisms.METHODS:In this study,we utilized cigarette smoke(CS)exposure and lipopolysaccharide(LPS)-induced models of COPD in rats to evaluate the effects of the JYTR on airway inflammation.Sprague-Dawley rats were randomly assigned to various groups:control,model,budesonide,synbiotics,and low,medium,and high JYTR.Pulmonary function was gauged using an animal volumetric tracer.Pathological alterations in lung tissue were examined under a light microscope.To ascertain cytokine production,we conducted enzyme-linked immunosorbent assay tests,and we employed Western blotting to measure the expression levels of interferon regulatory factor 4(IRF4),arginase 1(Arg1),inducible nitric oxide synthase(iNOS),nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor,alpha(IKB-α),and P65.RESULTS:Compared to the control group,rats in the COPD model group exhibited significantly compromised pulmonary function and severe inflammatory pathology in the lungs.Treatment with budesonide,synbiotics,and the JYTR markedly improved pulmonary function and diminished the production of inflammatory cytokines transforming growth factor-beta(TGF-β),tumor necrosis factor-alpha(TNF-α),and interleukin-6(IL-6).These improvements were particularly notable in the budesonide group and the high-dose JYTR group.Additionally,the JYTR increased the expression of IRF4 and upregulated the protein expression of Arg1,while concurrently downregulating the protein expression of iNOS,phosphorylated IKB-α,and phosphorylated P65.CONCLUSION:Our current study reveals that JYTR can mitigate inflammatory lung injury,enhance lung function,and lower levels of inflammatory cytokines induced by CS or LPS exposure in COPD model rats.The mechanism behind its anti-inflammatory effect likely involves the regulation of IRF4 expression and M2 polarization through the nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway. 展开更多
关键词 cigarette smoking inflammation pulmonary disease chronic obstructive interferon regulatory factors Jianpi Yifei Tongluo recipe
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Interferon regulatory factor 2 binding protein 2:a new player of the innate immune response for stroke recovery 认领 引用 被引量：1
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作者 Hsiao-Huei Chen Alexandre E R.Stewart 《Neural Regeneration Research》 SCIE CAS CSCD 2017年第11期1762-1764,共3页
Ischemic brain injury triggers an inflammatory response. tissue but can also exacerbate brain injury. Microglia are This response is necessary to clear damaged brain the innate immune cells of the brain that execute t... Ischemic brain injury triggers an inflammatory response. tissue but can also exacerbate brain injury. Microglia are This response is necessary to clear damaged brain the innate immune cells of the brain that execute this critical function. In healthy brain, microglia perform a housekeeping function, pruning unused syn- apses between neurons. However, microglia become activated to an inflammatory phenotype upon brain injury. Interferon regulatory factors modulate microglial activation and their production of inflammatory cytokines. This review briefly discusses recent findings pertaining to these regulatory mechanisms in the context of stroke recovery. 展开更多
关键词 interferon regulatory factors interferon beta protein 2 stroke inflammation synaptie pruning anxiety microglia interferon regulatory factor 2 binding
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Ropeginterferonα-2b治疗骨髓增殖性肿瘤的研究进展 认领 引用
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作者 屠玲榕 黄健 《中国实验血液学杂志》 CAS CSCD 北大核心 2025年第1期306-310,共5页
Ropeginterferonα-2b是新上市的一种长效聚乙二醇脯氨酸α干扰素,是第一种专门批准用于治疗真性红细胞增多症的干扰素,临床试验和经验发现其可以诱导骨髓增殖性肿瘤患者血液学缓解,控制疾病相关症状,降低JAK2V617F基因突变负荷。与聚... Ropeginterferonα-2b是新上市的一种长效聚乙二醇脯氨酸α干扰素,是第一种专门批准用于治疗真性红细胞增多症的干扰素,临床试验和经验发现其可以诱导骨髓增殖性肿瘤患者血液学缓解,控制疾病相关症状,降低JAK2V617F基因突变负荷。与聚乙二醇干扰素α和羟基脲相比,其药物不良反应发生率和严重程度较低,且给药间隔时间更长,部分低危真性红细胞增多症和骨髓纤维化患者也能从中获益。本文就Ropeginterferonα-2b在骨髓增殖性肿瘤中的最新研究进展作一综述。 展开更多
关键词 骨髓增殖性肿瘤 Ropeginterferonα-2b α干扰素 治疗
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Impact of hepatitis C virus heterogeneity on interferon sensitivity:An overview 认领 引用 被引量：5
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作者 Ahmed El-Shamy Hak Hotta 《World Journal of Gastroenterology》 SCIE CAS 2014年第24期7555-7569,共15页
Hepatitis C virus(HCV)is a major cause of liver disease worldwide.HCV is able to evade host defense mechanisms,including both innate and acquired immune responses,to establish persistent infection,which results in a b... Hepatitis C virus(HCV)is a major cause of liver disease worldwide.HCV is able to evade host defense mechanisms,including both innate and acquired immune responses,to establish persistent infection,which results in a broad spectrum of pathogenicity,such as lipid and glucose metabolism disorders and hepatocellular carcinoma development.The HCV genome is characterized by a high degree of genetic diversity,which can be associated with viral sensitivity or resistance(reflected by different virological responses)to interferon(IFN)-based therapy.In this regard,it is of importance to note that polymorphisms in certain HCV genomic regions have shown a close correlation with treatment outcome.In particular,among the HCV proteins,the core and nonstructural proteins(NS)5A have been extensively studied for their correlation with responses to IFN-based treatment.This review aims to cover updated information on the impact of major HCV genetic factors,including HCV genotype,mutations in amino acids 70 and91 of the core protein and sequence heterogeneity in the IFN sensitivity-determining region and IFNibavirin resistance-determining region of NS5A,on virological responses to IFN-based therapy. 展开更多
关键词 Hepatitis C virus Interferon Genotype Core protein Nonstructural proteins 5A Interferon sensitivity-determining region Interferonibavirin resistance-determining region
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Control of hepatitis B virus replication by interferons and Toll-like receptor signaling pathways 认领 引用 被引量：21
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作者 Rong-Juan Pei Xin-Wen Chen Meng-Ji Lu 《World Journal of Gastroenterology》 SCIE CAS 2014年第33期11618-11629,共12页
Hepatitis B virus (HBV) infection is one of the major causes of liver diseases, affecting more than 350 million people worldwide. The interferon (IFN)-mediated innate immune responses could restrict HBV replication at... Hepatitis B virus (HBV) infection is one of the major causes of liver diseases, affecting more than 350 million people worldwide. The interferon (IFN)-mediated innate immune responses could restrict HBV replication at the different steps of viral life cycle. Indeed, IFN-&#x003b1; has been successfully used for treatment of patients with chronic hepatitis B. However, the role of the innate immune response in HBV replication and the mechanism of the anti-HBV effect of IFN-&#x003b1; are not completely explored. In this review, we summarized the currently available knowledge about the IFN-mediated anti-HBV effect in the HBV life cycle and the possible effectors downstream the IFN signaling pathway. The antiviral effect of Toll-like receptors (TLRs) in HBV replication is briefly discussed. The strategies exploited by HBV to evade the IFN- and TLR-mediated antiviral actions are summarized. 展开更多
关键词 Hepatitis B virus Interferon Toll-like receptor Interferon stimulated genes Innate immune response
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DNA-dependent activator of interferon-regulatory factors inhibits hepatitis B virus replication 认领 引用 被引量：4
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作者 Qi-Ying Chen Ying-Hui Liu +3 位作者 Jian-Hua Li Ze-Kun Wang Jiang-Xia Liu Zheng-Hong Yuan 《World Journal of Gastroenterology》 SCIE CAS CSCD 2012年第22期2850-2858,共9页
AIM： To investigate whether DNA-dependent activator of interferon-regulatory factors （DAI） inhibits hepatitis B virus （HBV） replication and what the mechanism is. METHODS： After the human hepatoma cell line Huh7... AIM： To investigate whether DNA-dependent activator of interferon-regulatory factors （DAI） inhibits hepatitis B virus （HBV） replication and what the mechanism is. METHODS： After the human hepatoma cell line Huh7 was cotransfected with DAI and HBV expressing plas- mid, viral protein （HBV surface antigen and HBV e an- tigen） secretion was detected by enzyme-linked immu- nosorbent assay, and HBV RNA was analyzed by real- time polymerase chain reaction and Northern blotting, and viral DNA replicative intermediates were examined by Southern blotting. Interferon regulatory factor 3 （IRF3） phosphorylation and nuclear translocation were analyzed via Western blotting and immunofluorescence staining respectively. Nuclear factor-KB （NF-KB） activity induced by DAI was detected by immunofluorescence staining of P65 and dual luciferase reporter assay. Tran- swell co-culture experiment was performed in order to investigate whether the antiviral effects of DAI were dependent on the secreted cytokines. RESULTS： Viral protein secretion was significantly re- duced by 57% （P 〈 0.05）, and the level of total HBV RNA was reduced by 67% （P 〈 0.05）. The viral core particle-associated DNA was also dramatically down- regulated in DAI-expressing Huh7 cells. Analysis of involved signaling pathways revealed that activation of NF-KB signaling was essential for DAI to elicit antivi- ral response in Huh7 cells. When the NF-KB signaling pathway was blocked by a NF-KB signaling suppressor （I~：B^-SR）, the anti-HBV activity of DAI was remarkably abrogated. The inhibitory effect of DAI was indepen- dent of IRF3 signaling and secreted cytokines. CONCLUSION： This study demonstrates that DAI can inhibit HBV replication and the inhibitory effect is asso- ciated with activation of NF-KB but independent of IRF3 and secreted cytokines. 展开更多
关键词 DNA-dependent activator of interferon regu-latory factor Antiviral activity Hepatitis B virus Nuclearfactor-~B Interferon regulatory factor-3
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Hepatitis B surface antigen clearance in inactive hepatitis B surface antigen carriers treated with peginterferon alfa-2a 认领 引用 被引量：27
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作者 Ming-Hui Li Yao Xie +11 位作者 Lu Zhang Yao Lu Ge Shen Shu-Ling Wu Min Chang Cai-Qin Mu Lei-Ping Hu Wen-Hao Hua Shu-Jing Song Shu-Feng Zhang Jun Cheng Dao-Zhen Xu 《World Journal of Hepatology》 2016年第15期637-643,共7页
AIM: To examine the association between interferon(IFN) therapy and loss of hepatitis B surface antigen(HBs Ag) in inactive HBs Ag carriers. METHODS: This was a retrospective cohort study in inactive HBs Ag carriers, ... AIM: To examine the association between interferon(IFN) therapy and loss of hepatitis B surface antigen(HBs Ag) in inactive HBs Ag carriers. METHODS: This was a retrospective cohort study in inactive HBs Ag carriers, who were treatment-naive, with a serum HBs Ag level < 100 IU/m L and an undetectable hepatitis B virus(HBV) DNA level(< 100 IU/m L). All the 20 treated patients received subcutaneous PEG-IFN alfa-2a 180 μg/wk for 72 wk and were then followed for 24 wk. There were 40 untreated controls matched with 96 wk of observation. Serum HBs Ag, HBV DNA, and alanine aminotransferases were monitored every 3 mo in the treatment group and every 3-6 mo in the control group. RESULTS: Thirteen(65.0%) of 20 treated patients achieved HBs Ag loss, 12 of whom achieved HBs Ag seroconversion. Mean HBs Ag level in treated patients decreased to 6.69 ± 13.04 IU/m L after 24 wk of treatment from a baseline level of 26.22 ± 33.00 IU/m L. Serum HBV DNA level remained undetectable(< 100 IU/m L) in all treated patients during the study. HBs Ag level of the control group decreased from 25.72 ± 25.58 IU/m L at baseline to 17.11 ± 21.62 IU/m L at week 96(P = 0.108). In the control group, no patient experienced HBs Ag loss/seroconversion, and two(5.0%) developed HBV reactivation.CONCLUSION: IFN treatment results in HBs Ag loss and seroconversion in a considerable proportion of inactive HBs Ag carriers with low HBs Ag concentrations. 展开更多
关键词 Chronic hepatitis B surface antigen carriers Inactive hepatitis B surface antigen carriers Interferon Peginterferon alfa-2a Hepatitis B surface antigen loss/ seroconversion
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