Immunologic Research最新文献

{"title":"Role of basophils and type 2 inflammation in bullous pemphigoid pathophysiology: a comparative study of blood and blister fluid.","authors":"Bintao Su, Quanhong Zhang, Xianyong Hu, Bo Xie, Chao Chen, Yan Zhao, Zhi Liu, Ling Ma, Jinbo Chen","doi":"10.1007/s12026-025-09617-6","DOIUrl":"https://doi.org/10.1007/s12026-025-09617-6","url":null,"abstract":"<p><p>Bullous pemphigoid (BP) is an autoimmune disease characterized by blister formation and inflammatory cell infiltration. In addition to eosinophil and neutrophil infiltration, there are many other inflammatory cells and factors involved in the pathophysiology of BP. Elucidating the inflammation environment will help to the diagnosis and treatment of BP. We used flow cytometry and wright-stained smears to analyze immune cells, and cytometric bead array methods were used to analyze immune factors in matched blood and blister fluid. Besides abundant eosinophil and neutrophil accumulation, distinct basophil infiltration was detected in blister fluid of patients with BP. We also found significant CD4⁺ T lymphocyte activation and increased type 2 cytokine secretion in BP blister fluid. Under no stimulation, basophils produce more IL-4 compared to CD4⁺ T lymphocytes in BP blister fluid. Basophils might play a more important role in BP than we early thought. Along with other inflammatory cells and factors, basophils, demonstrated as one of the main producers of IL-4, orchestrate the type 2 inflammation environment in BP.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"68"},"PeriodicalIF":3.3,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HBx/WDR5 enhances IGF-1 transcription in hepatocellular carcinoma cells and promotes recruitment, infiltration, and activity of Treg cells.","authors":"Erli Wang, Shuhua Sun, Hui Li, Yi Jia, Zhe Bai","doi":"10.1007/s12026-025-09620-x","DOIUrl":"https://doi.org/10.1007/s12026-025-09620-x","url":null,"abstract":"<p><p>HBV X protein (HBx), the smallest open reading frame in the hepatitis B virus (HBV) genome, can promote hepatocellular carcinoma (HCC) tumorigenesis by activating the expression of multiple oncogenes through inducing epigenetic alterations and interacting with the underlying transcriptional machinery. HBV non-infected HepG2 and Huh7 cells were transfected with HBx expression plasmids. The transcriptional, protein expression, and secretion levels of IGF-1 were detected by RT-qPCR, western blot, and ELISA, respectively. ChIP-qPCR was used to analyze the binding proteins on the IGF-1 gene. A co-culture system of HCC and Treg cells was designed using Transwell chambers. IGF-1 mRNA, protein, and secretion levels were increased in HepG2 and Huh7 cells exogenously expressing HBx. HBx was able to enter the nucleus and interact with the enhancer region of the IGF-1 gene. Levels of WDR5 and H3K4me1, which bind to the enhancer region of the IGF-1 gene, were also increased in HepG2 and Huh7 cells ectopically expressing HBx. Knockdown of WDR5 counteracted the upregulation of IGF-1 mRNA and protein levels by HBx. In the cell co-culture system, HBx/IGF-1 signaling in HCC cells promoted Treg cells expansion, IL-10 secretion, and infiltration, which was blocked by the IGF-1R inhibitor picropodophyllin. HBx/WDR5 promoted IGF-1 transcription in HCC cells through enhancers. HBx could promote Treg cell recruitment, infiltration, and activity by enhancing IGF-1 expression. IGF-1/IGF-1R signaling plays an important role in the communication between HCC cells and Treg cells. Targeting WDR or IGF-1/IGF-1R would be beneficial for the treatment of HCC.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"69"},"PeriodicalIF":3.3,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phenotypic characterization of tumor associated macrophages and circulating monocytes in patients with Urothelial carcinoma of bladder.","authors":"Aishwarya Singh, David Raja, Seema Kaushal, Amlesh Seth, Prabhjot Singh, Alpana Sharma","doi":"10.1007/s12026-025-09624-7","DOIUrl":"https://doi.org/10.1007/s12026-025-09624-7","url":null,"abstract":"<p><strong>Objectives: </strong>Targeting immune checkpoints has shown clinical efficacy in Urothelial carcinoma of bladder (UBC); however, a substantial percentage of patients remains unresponsive, which warrants the elucidation of novel therapeutic targets to circumvent immune suppression. Tumor associated macrophages (TAMs) are known for their indispensable role in cancer immunosuppression however, their phenotype and functionality in UBC is not yet clear.</p><p><strong>Materials and methods: </strong>Phenotypic composition and functional markers of TAMs, and circulating monocytes were assessed in surgically resected bladder tumors and PBMC of UBC patients (n = 40). Besides, 40 healthy volunteers were recruited to draw comparisons for peripheral monocytes. Monocytes from patients were treated with autologous bladder tumor conditioned media (TCM) to assess its effects on macrophage-based markers.</p><p><strong>Results: </strong>The infiltration of TAMs was significantly increased in bladder tumor tissue by 21.2% and which displayed both M1 and M2 phenotypic markers, wherein M2 phenotype exhibited positive correlation with disease severity. Circulating monocytes exhibited an increase in frequency of non-classical monocytes by 17.42% and elevated M2-macrophage markers by 20%. Further, TAMs and circulating monocytes exhibits an elevated expression of IL- 10 and inhibitory immune checkpoints (PD-1, PD-L1, and B7-H4). Stimulation of patient-derived monocytes with TCM further augmented the expression of immune checkpoints, and immunosuppressive markers like IL-10, TGF-β and CX3CR- 1. Lastly, M2 phenotype of TAMs and PD-L1+ and B7-H4 + TAMs displayed positive correlation with clinico-pathological parameters in UBC patients.</p><p><strong>Conclusion: </strong>This study presents TAMs with an immunosuppressive phenotype that correlates positively with disease severity and suggests TAMs as a potential therapeutic candidate to restore the anti-tumor immunity in UBC.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"66"},"PeriodicalIF":3.3,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143803127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical management of autoimmune liver diseases: juncture, opportunities, and challenges ahead.","authors":"Yangfan Chen, Ruofei Chen, Haiyan Li, Zongwen Shuai","doi":"10.1007/s12026-025-09622-9","DOIUrl":"10.1007/s12026-025-09622-9","url":null,"abstract":"<p><p>The three major autoimmune liver diseases are autoimmune hepatitis (AIH), primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC).These conditions are assumed to result from a breakdown in immunological tolerance, which leads to an inflammatory process that causes liver damage.The self-attack is started by T-helper cell-mediated identification of liver autoantigens and B-cell production of autoantibodies,and it is maintained by a reduction in the number and activity of regulatory T-cells.Infections and environmental factors have been explored as triggering factors for these conditions, in addition to a genetic predisposition.Allelic mutations in the HLA locus have been linked to vulnerability, as have relationships with single nucleotide polymorphisms in non-HLA genes.Despite the advances in the management of these diseases, there is no curative treatment for these disorders, and a significant number of patients eventually progress to an end-stage liver disease requiring liver transplantation.In this line, tailored immune-therapeutics have emerged as possible treatments to control the disease.In addition, early diagnosis and treatment are pivotal for reducing the long-lasting effects of these conditions and their burden on quality of life.Herein we present a review of the etiology, clinical presentation, diagnosis, and challenges on ALDs and the feasible solutions for these complex diseases.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"67"},"PeriodicalIF":3.3,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143803125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pivotal epitopes for islet antigen-specific CD8⁺ T cell detection improve classification of suspected type 1 diabetes with the HLA-A*0201 allele.","authors":"Yang Chen, Min Shen, Yong Gu, Xinyu Xu, Lingling Bian, Fan Yang, Shuang Chen, Li Ji, Jin Liu, Jing Zhu, Zheng Zhang, Qi Fu, Yun Cai, Heng Chen, Kuanfeng Xu, Min Sun, Xuqin Zheng, Jie Shen, Hongwen Zhou, Mei Zhang, Kathryn Haskins, Liping Yu, Tao Yang, Yun Shi","doi":"10.1007/s12026-025-09616-7","DOIUrl":"https://doi.org/10.1007/s12026-025-09616-7","url":null,"abstract":"<p><p>A proportion of patients with new-onset diabetes share similar symptoms with type 1 diabetes (T1D) patients but they are negative for islet antigen-specific autoantibodies. This study was to develop an islet antigen-specific CD8⁺ T-cell assay to provide autoimmune evidence regarding these \"suspected\" T1D patients. HLA-A*0201 individuals with autoAbs⁺ T1D, autoAbs^- suspected T1D, and type 2 diabetes, along with HLA-A*0201 healthy controls were recruited. Using interferon-γ enzyme-linked immunospot assays, the percentages of participants in each group with various islet antigen-specific CD8⁺ T cells were determined. Sixteen out of the 28 islet antigen-specific epitopes tested were T1D specific, meaning that there was a significantly (P < 0.05) greater epitope positivity rate in the autoAbs⁺ T1D cohort than in the healthy controls. Using a cutoff value of two positive epitopes, the 16-epitope panel led to a sensitivity of 75.0% and a specificity of 94.4% regarding the autoAbs⁺ T1D patients. Even when using an optimized five-epitope panel, the results were highly accurate. Notably, in the application phase of the study, 77.8% of a new cohort of autoAbs^- suspected T1D patients exhibited positivity when using the five-epitope optimized panel. This highly accurate method, especially for pediatric patients, will improve clinical diagnosis and etiological classification of autoimmune T1D.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"65"},"PeriodicalIF":3.3,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143709747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"α-Amanitin aggravates hepatic injury by activating oxidative stress and mitophagy via peroxiredoxin 6 inhibition.","authors":"Zhongfeng Cheng, Kerun Cheng, Yan Tang, Xueqiong Duan, Yangshan Fu, Hongdan Duan, Yong Ye","doi":"10.1007/s12026-025-09619-4","DOIUrl":"https://doi.org/10.1007/s12026-025-09619-4","url":null,"abstract":"<p><p>Mushroom poisoning is mainly caused by α-amanitin (α-AMA), and there is currently no effective drug to treat α-AMA poisoning. Therefore, it is particularly important to find early diagnostic markers for α-AMA injury. Hepatic injury models induced by α-AMA were established both in hepatic cells and mice. The cell viability of human normal hepatic cells after α-AMA treatment was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Liver function parameters was assessed by the Enzyme-Linked Immunosorbent Assay (ELISA). Furthermore, oxidative stress was detected by 2',7'-Dichlorofluorescin Diacetate (DCFH-DA) and Dihydroethidium (DHE) staining. Autophagy- and apoptosis-related proteins were assessed by Western blot and immunofluorescence staining. We applied Hematoxylin and Eosin (H&E), Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and Oil Red O (ORO) staining to observe the degree of cell damage and hepatocyte apoptosis. In addition, mitochondrial membrane potential was also determined by JC-1 immunofluorescence staining and flow cytometry. The results showed that α-AMA decreased cell viability in a dose-dependent manner. In addition, the levels of alanine aminotransferase (ALT), aspartate transaminase (AST) and mitochondrial reactive oxygen species (mtROS) were observed to increase in the α-AMA-treated groups, whereas antioxidants superoxide dismutase (SOD) levels were reduced. Moreover, α-AMA promoted hepatocyte mitophagy and apoptosis, which were alleviated by PRDX6 overexpression. Finally, PRDX6 and Parkin were found to accumulate in mitochondria and α-AMA activated mitophagy by silencing PRDX6. Collectively, our results demonstrated that α-AMA activates oxidative stress and mitophagy by inhibiting the expression of PRDX6, leading to hepatic injury. These findings from both in vitro and in vivo models provide insights into the toxicological mechanisms of α-AMA, underscoring the potential of PRDX6 as a therapeutic target for treating α-AMA-induced hepatotoxicity. HIGHLIGHTS: α-AMA leads to ROS accumulation and activates oxidative stress. α-AMA promotes hepatocyte mitophagy and apoptosis. PRDX6 alleviates α-AMA-induced hepatic injury. PRDX6 mediates mitophagy through Parkin.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"64"},"PeriodicalIF":3.3,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Utility of simultaneous quantification of TREC/KREC in patients with common variable immunodeficiency phenotype: an observational study from North India.","authors":"Prabal Barman, Anit Kaur, Sanchi Chawla, Archan Sil, Manpreet Dhaliwal, Amit Rawat, Surjit Singh, Ankur Kumar Jindal","doi":"10.1007/s12026-025-09615-8","DOIUrl":"https://doi.org/10.1007/s12026-025-09615-8","url":null,"abstract":"<p><p>Because of its heterogeneity, common variable immunodeficiency (CVID), the commonest symptomatic inborn error of immunity, is difficult to classify. Limited data suggest T-cell receptor excision circles (TREC) and kappa-deleting re-combination excision circles (KREC) may be useful to better classify and prognosticate CVID and CVID phenotype. Thirty-four patients with CVID/CVID phenotype and 30 healthy controls were included in this cross-sectional observational study. Simultaneous quantification of TREC/KREC was performed using multiplex real-time polymerase-chain reaction with TaqMan probes. The levels of TREC/KRECs were analyzed for any association with clinical features, immunological investigations, and molecular studies. Median values of KREC and TREC copy numbers in patients with CVID/CVID phenotype were 64.5 and 170 copies/50 ng reaction, respectively, whereas the median values in controls were 79.2 and 190.1 copies/50 ng reaction respectively. We classified the patients into 4 groups based on copy numbers of TREC/KRECs: (A)TREC + /KREC + ; (B) TREC + /KREC-; (C) TREC-/KREC + ; (D)TREC-/KREC- [\" + \" and \" - \" denotes TREC/KREC levels above and below median value respectively]. Patients in Group B had higher risk of developing bronchiectasis. There was no significant difference vis-à-vis failure to thrive, infections, autoimmunity and malignancy, and levels of immunoglobulins, CD19⁺ B cells, and CD4:CD8 ratio amongst the 4 groups. Monogenic defects (n = 10/34) were more likely when age of onset was <math><mo>≤</mo></math> 4 years (p = 0.02), irrespective of TREC/KREC copy numbers. Classification of CVID/CVID phenotype based on TREC/KREC levels may not be feasible; however, a sub-group with low KREC/normal TREC levels may be predisposed to develop bronchiectasis. Patients with younger age of onset (< 4 years) were more likely to have monogenic defects.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"63"},"PeriodicalIF":3.3,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunoenhancing of the anti-cancer therapy and anti-oxidative stress by co-administration of granulocyte-colony stimulating factor-mobilized stem cells or cells derived from bone marrow and/or spleen plus vaccination with chemotherapeutic cyclophosphamide.","authors":"Soha Gomaa, Mohamed Nassef, Ghada Tabl, Shaimaa El Gabry","doi":"10.1007/s12026-025-09610-z","DOIUrl":"https://doi.org/10.1007/s12026-025-09610-z","url":null,"abstract":"&lt;p&gt;&lt;p&gt;The combination of immunotherapy and chemotherapy, referred to as chemo-immunotherapy, represents a promising regimen for developing new cancer treatments that target the local tumor microenvironment and target tumors in their early stages. However, this approach carries potential risks, including myelo- and immunosuppression, as well as the emergence of chemo-resistant tumor cells. The purpose of this study was to investigate how well mobilizing hematopoietic stem cells (HSCs) work when used alongside chemotherapy and immunotherapy to enhance and modulate the immune response, thereby overcoming immunosuppression and eliminating distant cancer cells. Ehrlich ascetic carcinoma (EAC) tumor-bearing mice were intraperitoneal (i.p.) preconditioned with CTX (4 mg/mouse). EAC-bearing mice that were preconditioned with CTX were intravenous (i.v.) administered with adoptive transferred naive mice-derived bone marrow cells (nBMCs) at 5 × 10&lt;sup&gt;6&lt;/sup&gt; through lateral tail vein (nBMCs group), adoptive transferred tumor-bearing mice-derived bone marrow cells (tBMCs) at 5 × 10&lt;sup&gt;6&lt;/sup&gt; cell/mouse (tBMCs group), a combination of adoptive transferred naïve mice-derived bone marrow cells (nBMCs) and naïve mice-derived splenocytes (nSPs) at 5 × 10&lt;sup&gt;6&lt;/sup&gt; (nBMCs/nSPs group), a combination of adoptive transferred tumor-bearing mice-derived bone marrow cells (tBMCs) and tumor-bearing mice derived-splenocytes (tSPs) at 5 × 10&lt;sup&gt;6&lt;/sup&gt; cell/mouse (tBMCs/tSPs group), or G-CSF administrated subcutaneously (s.c.) at 5 µg/mouse (G-CSF group). Subsequently, all mice groups were vaccinated with tumor lysate at a dosage of 100 µg/mouse. Treating EAC tumor-bearing mice with G-CSF, adoptive transferred nBMCs, adoptive transferred tBMCs, adoptive transferred nBMCs/nSPs, adoptive transferred tBMCs/tSPs, resulted in a significantly enhanced anti-tumor effect that was evidenced by increased anti-proliferative activity and growth inhibition against EAC tumor cells, increased necrosis and apoptosis rates among EAC tumor cells, restricted tumor growth in EAC tumor-bearing mice, and reduced levels of carcinoembryonic antigen (CEA) tumor marker. Furthermore, there was an improvement in serum levels of antioxidant enzyme superoxide dismutase (SOD) and malondialdehyde (MDA) in EAC tumor-bearing mice receiving G-CSF, adoptive transferred tBMCs, adoptive transferred nBMCs/nSPs, and adoptive transferred tBMCs/tSPs. Notably, this treatment regimen ameliorates liver and kidney damage associated with CTX administration in EA tumor-bearing mice. The integration of G-CSF-mobilized HSCs, adoptive transferred nBMCs, adoptive transferred tBMCs, adoptive transferred nBMCs/nSPs combination, and adoptive transferred tBMCs/tSPs combination may yield powerful anti-cancer therapy, thereby facilitating more effective anti-tumor immunotherapy strategies when align with anti-tumor responses. This research may propose a novel therapeutic approach that combines chemotherapy and immunotherapy","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"62"},"PeriodicalIF":3.3,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel loss of function mutation in the HAVCR2 gene in a patient diagnosed with Hodgkin's lymphoma.","authors":"Serife Erdem, Ebru Yilmaz, Alper Ozcan, Ahmed Nazim Canatan, Atil Bisgin, Muhammet Ensar Dogan, Musa Karakukcu, Ekrem Unal, Ahmet Eken","doi":"10.1007/s12026-025-09618-5","DOIUrl":"https://doi.org/10.1007/s12026-025-09618-5","url":null,"abstract":"","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"61"},"PeriodicalIF":3.3,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systemic barrier dysfunction in type 2 inflammation diseases: perspective in the skin, airways, and gastrointestinal tract.","authors":"Juan Meng, Hao Xiao, Feng Xu, Xueke She, Chuntao Liu, Giorgio Walter Canonica","doi":"10.1007/s12026-025-09606-9","DOIUrl":"10.1007/s12026-025-09606-9","url":null,"abstract":"<p><p>The epithelial barrier in different organs is the first line of defense against environmental insults and allergens, with type 2 immunity serving as a protective function. Genetic factors, and biological and chemical insults from the surrounding environment altered regulate epithelial homeostasis through disruption of epithelial tight junction proteins or dilated intercellular spaces. Recent studies suggest that epithelial barrier dysfunction contributes to pathologic alteration in diseases with type 2 immune dysregulation including (but not limited to) atopic dermatitis, prurigo nodularis, asthma, chronic rhinosinusitis with nasal polyps, and eosinophilic esophagitis. In this review, we summarized current understanding of dysfunction of barrier and its interaction with type 2 inflammation across different organs, and discussed the role of epithelial barrier disruption in the pathogenesis of type 2 inflammation. In addition, recent progresses of emerging barrier restorative therapies are reviewed.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"60"},"PeriodicalIF":3.3,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897119/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604751","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}