Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 25 2 2026 02 01 145 160 Daniel Karlsson School of Medical Science, Faculty of Medicine and Health, Örebro University, Örebro, Sweden Amanj Saber School of Medical Science, Faculty of Medicine and Health, Örebro University, Örebro, Sweden 2025 05 12 2025 08 02 Allergic disorders such as asthma, atopic dermatitis, and allergic rhinitis affect a large portion of the global population. The relationship between allergies and cancer has been studied extensively, but results remain inconsistent for head and neck cancer. The aim of this meta-analysis is to evaluate whether there is a negative association between allergic disorders and head and neck cancer. A systematic search of five databases was conducted based on Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Cohort- and case-control studies examining allergies and head and neck cancer were included. Random-effect and fixed-effect models were used to calculate pooled relative risk, with heterogeneity assessed via the I2 and Cochrane’s Q-test. Subgroup and sensitivity analyses were performed to explore variations by study design, allergy type, and cancer site. Twenty-five studies with 3.6 million participants were included. No significant overall association was found between allergic diseases and head and neck cancer (meta-RR: 0.89; 95% confidence intervals (CI): 0.76–1.05). Subgroup analyses revealed protective effects for asthma (meta-RR: 0.81; 95% CI: 0.70–0.95) and food allergies (meta-RR: 0.73; 95% CI: 0.54–0.99). Allergic rhinitis showed negative associations with oropharyngeal cancer (meta-RR: 0.76; 95% CI: 0.69–0.84) and hypopharyngeal cancer (meta-RR: 0.65; 95% CI: 0.55–0.78), but a positive association with nasopharyngeal cancer (meta-RR: 1.67; 95% CI: 1.15–2.43). These findings suggest complex relationships between allergies and head and neck cancer, with negative and positive associations varying by allergy type and cancer site. Further research is needed to clarify these associations. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/4442 https://ijaai.tums.ac.ir/index.php/ijaai/article/download/4442/2258

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 25 2 2026 02 01 251 263 Tao Liu Department of Respiration, The 80th Group Army Hospital of People’s Liberation Army, Weifang, China Na Zhang Department of Respiration, The 80th Group Army Hospital of People’s Liberation Army, Weifang, China Xin Shu Department of Dermatology, The Third Medical Center of Chinese PLA General Hospital, Beijing, China Xiaoxuan Hu Department of Pulmonary and Critical Care Medicine, Weifang No. 2 People’s Hospital, Weifang, China AND Institute of Toxicology and Pharmacology, Academy of Military Medical Sciences, Beijing, China Jingtong Li Department of Respiration, The 80th Group Army Hospital of People’s Liberation Army, Weifang, China Yuxu Zhong Institute of Toxicology and Pharmacology, Academy of Military Medical Sciences, Beijing, China Jinyuan Tang Department of Respiration, The 80th Group Army Hospital of People’s Liberation Army, Weifang, China Xiao-ji Zhu Department of Respiration, The 80th Group Army Hospital of People’s Liberation Army, Weifang, China 2025 04 06 2025 07 25 Sulfur mustard (SM) is a potent chemical warfare agent that causes severe cutaneous, ocular, and pulmonary injuries, with respiratory tract damage being the most life-threatening. Despite its well-documented toxicity, the cellular mechanisms driving SM-induced apoptosis remain poorly understood. This study seeks to elucidate the apoptotic pathways involved in SM-induced pulmonary injury using a rat model. We induced acute lung injury through two delivery methods: intraperitoneal injection (8 mg/kg) and intratracheal instillation (2 mg/kg) of SM, with both doses representing 1 LD50. We assessed apoptosis-related proteins and gene expression through TUNEL staining, immunohistochemistry, and quantitative real-time PCR analyses. Intraperitoneal administration of SM resulted in significantly elevated expression of apoptotic markers including annexin A1, annexin A2, cytochrome C, caspase-12, and JNK3, in alveolar epithelial cells compared to intratracheal delivery. Both TUNEL assays and immunohistochemical staining confirmed these findings. These results indicate that intraperitoneal SM exposure triggers more severe apoptotic responses in alveolar epithelial cells than intratracheal exposure at equivalent doses. These findings demonstrate that intraperitoneal models can effectively identify apoptosis-related molecular targets suitable for therapeutic development. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/4408 https://ijaai.tums.ac.ir/index.php/ijaai/article/download/4408/2235

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 25 2 2026 02 01 234 250 EN Hossein Rahavi Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran AND Stem Cell Biology Research Center, Yazd Reproductive Sciences Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran Ahmad Najafi SABA Biomedicals Knowledge-Enterprise Co, Tehran, Iran Hossein Asgarian-Omran Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran Behrouz Aflatoonian Stem Cell Biology Research Center, Yazd Reproductive Sciences Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran Mohsen Tehrani Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. Ehsan Farashahi-Yazd Stem Cell Biology Research Center, Yazd Reproductive Sciences Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. 2025 05 19 2025 08 01 Tumor microenvironment modulators have produced durable effects in cancer treatment. Targeting immune checkpoint receptors, such as PD-L1, has demonstrated efficacy in eliciting antitumor responses. However, resistance to immune checkpoint blockers (ICBs) has constrained the efficacy of these therapies. Previous studies showed a link between the expression of AXL receptor tyrosine kinase and resistance to ICBs. Therefore, designing combination treatments with synergistic mechanisms to overcome ICB-based resistance is needed. In addition to antibody-based therapies, gene silencing with siRNAs has recently been explored to alter the cancer environment to enhance the immune response. In this study, we targeted PD-L1 using an siRNA and AXL using a blocker (R428) in OVACAR-3 and CaSki cells, ovarian and cervical cancer cell lines, respectively, in the following groups: Scramble-siRNA, PD-L1-siRNA, Scramble-siRNA in conjunction with R428, PD-L1-siRNA in conjunction with R428, R428 monotherapy and untreated controls. Cell viability was assessed by MTT assay after 48 hours of treatment, and cisplatin sensitization was evaluated in resistant OVACAR-3 cells. Gene expression was analyzed by qRT-PCR, while flow cytometry quantified CD44+PD-L1+ populations, apoptosis (Annexin V/PI), and cell cycle distribution. The results showed a significant decrease in cell proliferation, suppression of EMT-regulating genes, reduction of stemness in cancer cells, increased apoptosis and disruption of the cell cycle in the studied cell lines. These findings suggest that simultaneous blockade of PD-L1 and AXL could serve as a novel tumor-suppressive strategy, especially for cancer patients resistant to ICBs. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/4448 https://ijaai.tums.ac.ir/index.php/ijaai/article/download/4448/2233

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 25 2 2026 02 01 222 233 EN Kaichong Jiang Shaanxi Institute for Pediatric Diseases, The Affiliated Children Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, China Qiao Li Clinical Laboratory, The Affiliated Children Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, China Ling Duan Department of Clinical Laboratory, The Affiliated Hospital of Yunnan University (The Second People's Hospital of Yunnan Province), Kunming, China Xieying Zhu Clinical Laboratory, The Affiliated Children Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, China Shuang Wu Clinical Laboratory, The Affiliated Children Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, China 2025 05 05 2025 09 04 Asthma is a chronic inflammatory disease characterized byimmune dysregulation. This study aimed to perform unbiased analysis of transcriptomic data to identify differentially expressed m6A-related genes in asthma, with a focus on exploring their potential as biomarkers and therapeutic targets. Gene Expression Omnibus (GEO) (GSE134544) dataset was analyzed to identify differentially expressed m6A-related genes. Functional enrichment analysis was performed clusterProfiler, immune infiltration profiling was conducted with CIBERSORT, and a competing endogenous RNA (ceRNA, including microRNA [miR] and lncRNA) network was constructed. Drug enrichment analysis was carried out using DSigDB, and molecular docking was utilized to assess the interaction between dabigatran and the METTL3 protein. From 192 differentially expressed genes, four m6A-related genes (METTL3, HNRNPC, IGFBP2, and RBMX) were identified as the intersecting genes between the m6A-related gene set and differentially expressed genes (DEGs) from the GSE134544 dataset. Gene Ontology (GO) analysis revealed significant enrichment in biological processes related to RNA metabolic processes and post-transcriptional regulation, while Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis identified important pathways such as spliceosome and p53 signaling pathways. METTL3 and HNRNPC were central in the ceRNA network, interacting with miRs such as hsa-miR-93-3p and lncRNAs like LINC01529. Drug enrichment analysis identified dabigatran as a potential METTL3 inhibitor, with molecular docking confirming a stable binding affinity (−5.9 kcal/mol). This study emphasizes the critical role of m6A-related genes, particularly METTL3 and HNRNPC, as macromolecules in asthma pathophysiology, and provides insights into their potential as biomarkers and therapeutic targets for asthma treatment. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/4433 https://ijaai.tums.ac.ir/index.php/ijaai/article/download/4433/2243

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 25 2 2026 02 01 212 221 Solmaz Aziz-Ahari Division of Pediatric Neurology, Pediatrics Center of Excellence, Children’s Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran Mahdi Aminian Department of Clinical Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran Aliasghar Rahimian Department of Clinical Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran Shahriar Nafissi 3 Neuromuscular Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran AND Department of Neurology, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran Morteza Heidari Division of Pediatric Neurology, Pediatrics Center of Excellence, Children’s Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran Ali Rabbani Growth and Development Research Center, Pediatrics Center of Excellence, Children’s Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran AND Department of Pediatric Endocrinology, Pediatric Center of Excellence, Children's Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran Amir-Hassan Zarnani Department of Pathobiology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran Ali Mohebbi Growth and Development Research Center, Pediatrics Center of Excellence, Children’s Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran Reza Shervin Badv Division of Pediatric Neurology, Pediatrics Center of Excellence, Children’s Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran Narges Salajegheh Medical Laboratory, Social Security Organization, Tehran, Iran Sahar Mortezagholi Department of Immunology, Shahid Beheshti University of Medical Sciences, Tehran, Iran Safdar Masoumi Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran Zahra Hadipour Department of Clinical Genetics, Atieh Hospital, Tehran, Iran Reza Boostani Department of Neurology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran Mehran Beiraghi Toosi Department of Pediatric Neurology, Ghaem Hospital, Mashhad University of Medical Sciences, Mashhad, Iran Keyhan Sayadpour Zanjani Division of Cardiology, Department of Pediatric, Pediatric Center of Excellence, Children’s Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran Ali Khajeh Department of Pediatric Neurology, Children and Adolescents Health Research Center, Zahedan University of Medical Sciences, Zahedan, Iran Seyed Hassan Tonkaboni Department of Pediatric Neurology, Shahid Beheshti University of Medical Sciences, Tehran, Iran Maryam Sadeghi Division of Pediatric Neurology, Pediatrics Center of Excellence, Children’s Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran Farzad Fatehi Department of Neurology, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran Elahe Vafaei Fetal and Pediatric Cardiovascular Research Center, Pediatric Center of Excellence, Children’s Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran Mahmoud Reza Ashrafi Division of Pediatric Neurology, Pediatrics Center of Excellence, Children’s Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran AND Neuromuscular Research Center, Shariati Hospital, Tehran and this immune improvement significantly optimizes clinical outcomes. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/4334 https://ijaai.tums.ac.ir/index.php/ijaai/article/download/4334/2244

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 24 6 2025 10 29 786 798 Neda Dalil Roofchayee Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran AND Clinical Tuberculosis and Epidemiology Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran AND Department of medicine, Northwestern University, Chicago, Illinois, USA Jalal Heshmatnia Chronic Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran Hamidreaza Jamatti Chronic Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran Mohammad Varahram Mycobacteriology Research Center (MRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran Ian Adcock Airways Disease Section, Faculty of Medicine, National Heart and Lung Institute, Imperial College London, London, United Kingdom Esmaeil Mortaz Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran AND Clinical Tuberculosis and Epidemiology Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran AND Chronic Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran 2024 08 27 2025 05 07 Idiopathic pulmonary fibrosis (IPF) is a severe lung disease with a poor prognosis, characterized by immune cell activation. The role of T helper (Th) cell transcription factors in IPF pathogenesis remains unclear. In this study, we investigated Th cell transcription factors and related cytokines in IPF patients. Twelve IPF patients and eight healthy controls (HC) were enrolled in this pilot study. Serum levels of fibrosis-associated mediators (Interferon-inducible protein 10 (IP-10), tumor necrosis factor-α (TNF-α), tumor growth factor-β (TGF-β), CXCL-8, interferon-γ (IFN-γ)) were measured by enzyme-linked immunosorbent assay (ELISA). Flow cytometry assessed Th transcription factors T box transcription factor (T-bet,), GATA-binding protein 3 (GATA-3), Retinoic acid-related orphan recepto (ROR-γt), forkhead box P3 (FOXP3)) and intracellular cytokines (IL-4, IL-17). SerumTGF-β, CXCL-8, TNF-α, and IFN-γ were significantly elevated, while IP-10 (pT-bet, GATA3, ROR-γt, or FOXP3 were observed. Positive correlations were found between T-bet and GATA3, IL-4, ROR-γt, and TNF-α expression with age, while FOXP3 expression negatively correlated with age. T-cell transcription factors were unchanged in IPF despite changes in inflammatory protein expression. Reduced IP-10 may serve as a potential marker. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/4185 https://ijaai.tums.ac.ir/index.php/ijaai/article/download/4185/2245

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 24 6 2025 10 29 799 807 EN Maryam Moradi Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Mahsa Yousefpour Marzbali Research Center for Immunodeficiencies, Children’s Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran Nazanin Nazari Shiraz Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran Zahra Chavoshzadeh Department of Allergy and Clinical Immunology, Mofid Children’s Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran Seyed Alireza Mahdaviani St. Giles Laboratory of Human Genetics of Infectious Disease, The Rockefeller University, New York, NY, USA AND Paris Cite University, Imagine Institute, Paris, France, EU AND Pediatric Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran Mahnaz Sadeghi-Shabestari Immunology Research Center of Tabriz, Mardaniazar Children Hospital of Tabriz, Tabriz University of Medical Sciences, Tabriz, Iran Nima Rezaei Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran AND Research Center for Immunodeficiencies, Children’s Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran AND Network for Immunology in Infection, Malignancy, And Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran 2024 12 04 2025 04 23   The autosomal recessive form of hyperimmunoglobulin E syndrome (AR-HIES), caused by mutations in the DOCK8 (Dedicator of Cytokinesis 8) gene, presents a wide range of clinical manifestations and phenotypically overlaps with several types of combined immunodeficiency disorders characterized by elevated serum IgE levels. Due to the high rates of morbidity and mortality, as well as the potential curability through hematopoietic stem cell transplantation (HSCT), early and accurate differential diagnosis of this syndrome is crucial for optimal management and improved prognosis. Flow cytometry tests can be beneficial for early diagnosis of many inborn errors of immunity (IEIs), including this syndrome. This study, conducted for the first time on Iranian patients, investigated the expression of the DOCK8 protein. DOCK8 expression was assessed by flow cytometry in 14 patients (6 males and 8 females) with a clinical diagnosis of DOCK8 deficiency. The diagnosis was ultimately confirmed through genetic testing. The results showed that DOCK8 expression in patients was significantly lower compared to the healthy control group. Flow cytometric evaluation of DOCK8 protein expression offers a rapid and efficient diagnostic method with a sensitive detection range suitable for many cases. This approach can facilitate the diagnosis of DOCK8 deficiency, thereby enabling timely and effective disease management.  https://ijaai.tums.ac.ir/index.php/ijaai/article/view/4267 https://ijaai.tums.ac.ir/index.php/ijaai/article/download/4267/2246

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 24 6 2025 10 29 808 817 Rong Li Department of Obstetrics and Gynecology, Tangdu Hospital, Air Force Medical University, Xi’an, 710038, Shaanxi China. Ying Yan Department of Obstetrics and Gynecology, Tangdu Hospital, Air Force Medical University, Xi’an, 710038, Shaanxi China. Fei Liu Department of Obstetrics and Gynecology, Tangdu Hospital, Air Force Medical University, Xi’an, 710038, Shaanxi China. Xiaoyu Gao Department of Obstetrics and Gynecology, Tangdu Hospital, Air Force Medical University, Xi’an, 710038, Shaanxi China. Xianling Fu Department of Obstetrics and Gynecology, Tangdu Hospital, Air Force Medical University, Xi’an, 710038, Shaanxi China. Luona Hu Department of Obstetrics and Gynecology, Tangdu Hospital, Air Force Medical University, Xi’an, 710038, Shaanxi China. Yanhong Li Department of Obstetrics and Gynecology, Tangdu Hospital, Air Force Medical University, Xi’an, 710038, Shaanxi China. 2025 05 29 2025 06 16 This study aimed to investigate the expression patterns of HOXB9, DLX5, NGR1, and GATA6 in endometrial cancer tissues compared to adjacent non-cancerous tissues. Using RT-qPCR and immunohistochemistry, the researchers found significant upregulation of HOXB9, DLX5, and NGR1, and downregulation of GATA6 in endometrial cancer samples. The biomarker expression levels correlated with clinicopathological features, and survival analysis revealed that high expression of HOXB9, DLX5, and NGR1 was associated with poorer prognosis, while high GATA6 expression indicated better outcomes. These findings suggest that these biomarkers may play crucial roles in endometrial cancer development and progression, highlighting their potential as diagnostic, prognostic, and therapeutic targets. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/4469 https://ijaai.tums.ac.ir/index.php/ijaai/article/download/4469/2247

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 24 6 2025 10 29 818 833 Maryam Rezaeezade_Roukerd Department of Basic Sciences, Faculty of Veterinary Medicine, Shahid Bahonar University of Kerman, Kerman, Iran Manijeh Dogani Department of Biology, Faculty of Sciences, Shahid Bahonar University of Kerman, Kerman, Iran Sahel Motaghi Department of Basic Sciences, Faculty of Veterinary Medicine, Shahid Bahonar University of Kerman, Kerman, Iran Mehdi Abbasnejad Department of Biology, Faculty of Sciences, Shahid Bahonar University of Kerman, Kerman, Iran 2025 02 04 2025 02 25 Spinal cord injuries (SCI) lead to complex primary and secondary damage that disrupts neural function. Current treatments are often insufficient and unable to fully repair spinal cord injuries, highlighting the urgent need for new medicines and innovative therapies. This study aimed to evaluate the therapeutic potential of abscisic acid (ABA) in SCI by examining its effects on immune-inflammatory genes’ expression in rats. This phytohormone possesses anti-inflammatory and neuroprotective properties, rendering it a potential agent for reducing secondary damage following spinal cord injury. Additionally, we performed protein-protein interaction (PPI), pathway enrichment, functional annotation, and gene ontology (GO) analyses to gain a comprehensive understanding of the functions of the affected genes. Based on the results, SCI led to changes in the expression of immune/inflammation-related genes in rats. However, the administration of ABA alleviated the effects. ABA downregulated proinflammatory genes (IL-6, IL-1β, MCP, TLR2, TLR4) and neural signaling components (NMDA, AMPA, NK1R), while upregulating adrenergic receptors (ADRA1A, ADRB1) and a gamma-aminobutyric acid receptor (AGBRA2). PPI analysis identified FOS, IL-1β, IL-6, MMP9, and TLR4 as crucial nodes in the network, exhibiting the highest degree of interaction. Functional analyses revealed potential impacts on cellular responses, metabolic processes, and synapse-associated extracellular matrix components. Notably, these genes were enriched in inflammatory signaling pathways according to KEGG analysis. These findings suggest that ABA has a significant modulatory effect on gene expression following SCI, particularly in reducing inflammation and immune responses, thereby highlighting its potential as a novel therapeutic agent for SCI. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/4329 https://ijaai.tums.ac.ir/index.php/ijaai/article/download/4329/2249

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 24 6 2025 10 29 834 850 Mi Xiang Department of Obstetrics, Puren Hospital Affiliated to Wuhan University of Science and Technology, Wuhan, China Yi Yu Department of Obstetrics, Puren Hospital Affiliated to Wuhan University of Science and Technology, Wuhan, China Qin Gao Department of Obstetrics and Gynecology, Puren Hospital Affiliated to Wuhan University of Science and Technology, Wuhan, China Jie Xing Department of Obstetrics, Puren Hospital Affiliated to Wuhan University of Science and Technology, Wuhan, China 2025 01 08 2025 04 19 MicroRNA (miR)-425-5p is used as a molecular biomarker to identify cervical cancer (CxCa). However, few studies have examined the miR-425-5p-based modulation of the vital activities of CxCa cells. The levels of neural cell adhesion molecule 1 (NCAM1) and miR-425-5p in CxCa tissues and cells were tested using western blot and reverse transcription quantitative polymerase chain reaction (RT-qPCR) tests. CxCa cells’ malignant phenotype was examined through clone formation tests, and transwell tests. CD8+T cells were co-cultured with CxCa cells and then analyzed for apoptosis rates and the expression of activation proteins (granzyme B (GZMB) and perforin) as well as immune factors (tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ)) using flow cytometry, western blot, and enzyme-linked immunosorbent assay (ELISA) methods. Finally, in nude mouse experiments, the tumor size was measured for subcutaneous tumors, and the expression of CD8+T cell-related factors was detected. The NCAM1 and miR-425-5p were down-regulated and up-regulated in CxCa tissue and cells, respectively. After silencing miR-425-5p, CxCa cells showed attenuation in vitality, clone formation rate, and their capacities to migrate, penetrate, and evade immune responses. NCAM1 was targeted and silenced by miR-425-5p. When NCAM1 was silenced, it partially counteracted miR-425-5p’s inhibitory effects on the immune escape and proliferation. In nude mice, the tumor size and weight decreased after silencing miR-425-5p, and levels of CD8, IFN-γ, TNF-α, perforin, and GZMB were elevated. However, these changes were reversed when NCAM1 was silenced. In conclusion, miR-425-5p mediates the biological behavior and immune evasion of CxCa cells by regulating NCAM1. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/4302 https://ijaai.tums.ac.ir/index.php/ijaai/article/download/4302/2250

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 24 6 2025 10 29 851 859 Zhaomei Xu Clinical Laboratory, Tiantai People’s Hospital, Zhejiang, China Yanan Zhang Clinical Laboratory, Tiantai People’s Hospital, Zhejiang, China Jinfei Pang Department of Gynecology and Obstetrics, Tiantai People’s Hospital, Zhejiang, China Xiao Chen Clinical Laboratory, Tiantai People’s Hospital, Zhejiang, China Yulong Chen Clinical Laboratory, Tiantai People’s Hospital, Zhejiang, China Yafei Chen Clinical Laboratory, Tiantai People’s Hospital, Zhejiang, China Yingwei Wang Clinical Laboratory, Tiantai People’s Hospital, Zhejiang, China 2024 11 20 2025 02 13 This study aims to investigate the role of notopterol in alleviating endometritis induced by lipopolysaccharide (LPS) and to explore its underlying mechanisms.Human endometrial epithelial cells (hEECs) were treated with LPS to establish an in vitro model of endometritis, and the cells were divided into five groups: control, LPS, LPS+notopterol(15 mol/L), LPS+notopterol(305 mol/L) and LPS+notopterol(45 mol/L) groups. The expression levels of inflammatory factors were determined by Enzyme-Linked ImmunoSorbent Assay (ELISA). Apoptosis was detected by TdT-mediated dUTP Nick-End Labeling (TUNEL) method. Cell viability was determined by Cell Counting Kit-8 (CCK-8) test. Western blot was used to detect the expression levels of nuclear factor κB(NF-κB) p65, NF-κB inhibitor (IκBα), p-NF-κB p65 and p-IκBα. Following LPS treatment, cytokine levels significantly increased compared to the control group.; moreover, cell proliferation decreased, apoptosis increased, and the expression level of p-NF-κB p65 was increased. Subsequently, the LPS-treated hEECs were exposed to notopterygium. Compared to the LPS group. Treatment with LPS + notopterol resulted in a dose-dependent reduction in inflammatory cytokines, increased cell proliferation, and a significant reduction in apoptosis. Furthermore, the expression levels of p-NF-κB p65 and p-IκBα were downregulated. These findings suggest that notopterol alleviates LPS-induced endometritis by inhibiting the TLR4/NF-κB signaling pathway. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/4249 https://ijaai.tums.ac.ir/index.php/ijaai/article/download/4249/2251

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 24 6 2025 10 29 749 759 Dan Lei Department of Pediatrics, The First People’s Hospital of Changde, Changde, Hunan, China Yihu Liu Department of Pediatrics, The Fourth People's Hospital of Changde, Changde, Hunan, China Man Liu Department of Pediatrics, The First People’s Hospital of Changde, Changde, Hunan, China 2025 02 25 2025 05 08 Adenovirus infection is a common cause of pediatric respiratory disease, often misdiagnosed as a bacterial infection. This study compared immune-inflammatory markers in children with adenovirus- vs bacterial-induced suppurative tonsillitis and evaluated their correlation with adenovirus pneumonia. A retrospective study of 275 children (145 with adenovirus, 130 with bacterial infections) admitted to The First People’s Hospital of Changde, China (January–June 2019), was conducted. Laboratory markers (white blood cell [WBC] count, C-reactive protein [CRP], serum amyloid A [SAA], procalcitonin [PCT], heparin-binding protein [HBP], tumor necrosis factor-alpha [TNF-α], and interleukin 6 [IL-6]) were analyzed. Adenovirus cases were stratified by pneumonia status (58 with pneumonia, 87 without pneumonia) via chest computed tomography. Compared with the bacterial group, the adenovirus group had lower WBC counts (14.97 [1.37] vs 18.86 [2.65] ×109/L), CRP levels (15.26 [3.44] vs 26.36 [3.18] mg/L), and PCT levels (15.06 [2.12] vs 42.53 [4.58] ng/L) but higher SAA levels (216.75 [39.23] vs 136.55 [28.66] mg/L). Among children with adenovirus, those with pneumonia had elevated SAA (236.39 [38.67] vs 203.65 [33.95] mg/L), HBP (44.30 [8.93] vs 35.62 [6.77] ng/mL), TNF-α (731.52 [99.21] vs