Cellular immunology最新文献

{"title":"MEX3A activates the JAK-STAT pathway to suppress NK cell cytotoxicity and accelerate lung adenocarcinoma progression","authors":"Jigui Peng ,&nbsp;Haiqiang Yan ,&nbsp;Wang Zhou ,&nbsp;Hui Chen ,&nbsp;Tao Xu ,&nbsp;Changjin He","doi":"10.1016/j.cellimm.2025.104994","DOIUrl":"10.1016/j.cellimm.2025.104994","url":null,"abstract":"<div><h3>Background</h3><div>Therapeutic potential of natural killer (NK) cells is recognized in treating lung adenocarcinoma (LUAD), but impairment of NK cell functions in various cancers weakens anti-tumor capabilities. Uncovering molecular mechanisms is imperative for fortifying NK cells against degradation and for enhancing their cancer-inhibiting functions.</div></div><div><h3>Methods</h3><div>TCGA-LUAD database complemented by qRT-PCR presented MEX3A expression in LUAD. TIMER was employed to explore relationship between MEX3A levels and NK cell infiltration. In the co-culture system of LUAD and activated NK92 cells, CytoTox 96® assay was applied to gauge NK cell cytotoxicity. ELISA was used to quantify IFN-γ, Perforin, and Granzyme B in the supernatant. Flow cytometry assessed LUAD cell apoptosis. Single-gene enrichment analysis of MEX3A was performed with KEGG database. Western blot examined protein expression in JAK-STAT signaling. In vivo studies validated the role of MEX3A expression on tumorigenesis.</div></div><div><h3>Results</h3><div>MEX3A was upregulated in LUAD tissue and cells, negatively linked to NK cell infiltration levels. Gene set enrichment analysis pointed to influences of MEX3A expression on dynamics of JAK-STAT signaling. MEX3A overexpression in LUAD cells impaired NK cell cytotoxicity and cell apoptosis, and these effects were reversible by a JAK pathway inhibitor. Mouse studies illustrated that LUAD progression was curbed by MEX3A suppression, alongside an enhanced presence of NK cells within tumor microenvironment.</div></div><div><h3>Conclusion</h3><div>To synthesize our results, this study identified that MEX3A in LUAD promoted malignancy of the disease by enhancing JAK-STAT signaling, which in turn inhibited cytotoxic capabilities of NK cells, thus providing novel insights for LUAD immunotherapy.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"414 ","pages":"Article 104994"},"PeriodicalIF":3.7,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307342","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":"Polymorphonuclear myeloid-derived suppressor cells protect against hyperoxia-induced bronchopulmonary dysplasia in neonatal mice through suppression of excessive inflammatory response","authors":"Boshi Yu,&nbsp;Guixuan Hong,&nbsp;Yubai Li,&nbsp;Xudong Yan,&nbsp;Zhangbin Yu","doi":"10.1016/j.cellimm.2025.104995","DOIUrl":"10.1016/j.cellimm.2025.104995","url":null,"abstract":"<div><h3>Background</h3><div>Bronchopulmonary dysplasia (BPD), which primarily affects premature infants, is characterized by impaired lung development, reduced alveolarization, and chronic inflammation, leading to long-term respiratory complications. However, clinical prevention treatment of BPD remains challenging. Because immune cells may have a role in BPD pathogenesis and prevention, we investigated whether polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) protect against hyperoxia-induced BPD in a neonatal mouse model.</div></div><div><h3>Methods</h3><div>Neonatal C57BL/6 mice were exposed to either normoxia (21 % oxygen) or hyperoxia (85 % oxygen) since birth. Lung development was analyzed on postnatal days 3, 7, and 14 by using histological techniques [hematoxylin and eosin (H&amp;E) staining and radial alveolar count (RAC) measurement]. Moreover, we used flow cytometry to identify lung myeloid-derived suppressor cell (MDSC) subsets. PMN-MDSCs' therapeutic potential at key developmental stages was evaluated through adoptive transfer experiments. PMN-MDSC transplantation outcomes in the lung tissues were assessed through histological analysis, immunofluorescence staining for alveolar and vascular markers, and proinflammatory cytokine measurement.</div></div><div><h3>Results</h3><div>Hyperoxia-exposed mice exhibited considerable lung damage, including enlarged and irregular alveoli, low RACs, and decreased body weights compared with normoxic controls. Hyperoxia reduced PMN-MDSC numbers but increased monocytic MDSC numbers. PMN-MDSC transplantation preserved alveolar structure and increased alveolar and pulmonary vessel numbers. Immunofluorescence staining confirmed enhanced alveolar and vascular development. Finally, PMN-MDSCs reduced proinflammatory cytokine levels in lung tissues.</div></div><div><h3>Conclusion</h3><div>PMN-MDSCs may protect against hyperoxia-induced lung injury by promoting alveolar and vascular development and reducing inflammation in neonatal mice. Further research elucidating precise mechanisms underlying the protective effects of PMN-MDSCs and their potential for clinical translation is warranted.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"414 ","pages":"Article 104995"},"PeriodicalIF":3.7,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144280815","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":"Efficacy and safety of interferon alpha-2b aerosol therapy for patients infected with the SARS-CoV-2 omicron variant: A randomized controlled single-blind study","authors":"Yinpeng Jin ,&nbsp;Xianming Meng ,&nbsp;Zhiping Qian ,&nbsp;Jun Zhao ,&nbsp;Ying Lv ,&nbsp;Yun Ling ,&nbsp;Xiaohong Fan","doi":"10.1016/j.cellimm.2025.104992","DOIUrl":"10.1016/j.cellimm.2025.104992","url":null,"abstract":"<div><div>The efficacy of Type I interferon (IFN) in treating COVID-19 has remained controversial. In this study, we conducted a randomized, single-blind clinical trial to evaluate the efficacy of recombinant human interferon alpha 2b (IFN-alpha2b) in treating COVID-19 patients during the Omicron outbreak in Shanghai in 2022. The study cohort included 505 patients, classified as asymptomatic, mild, or moderate based on clinical symptoms. The cohort was divided into an experimental group, which received a 7-day course of nebulized inhalation of IFN-alpha2b, and a control group, which received an identical treatment course using physiological saline in place of IFN-alpha2b. Effectiveness and safety were assessed by measuring the length of hospital stay, improvement in clinical symptoms, and occurrence of adverse events. While there were no significant differences in overall hospital stay or symptom improvement between the two groups, IFN-alpha2b treatment was associated with a significantly shorter hospitalization time in the asymptomatic subgroup. Multivariate Cox regression analysis identified IFN nebulization therapy as a positive predictor of discharge within 12 days, alongside the white blood cell count at admission, and the IL-4 level at admission as a potential negative predictor. Regarding safety, there was no significant difference in the incidence of adverse reactions between the two groups during treatment. Collectively, our study suggests that Type I IFN, when administered via nebulized inhalation, may offer benefits specifically for the asymptomatic subgroup among COVID-19 patients, indicating selective efficacy.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"414 ","pages":"Article 104992"},"PeriodicalIF":3.7,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144364751","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":"Gliadin amplifies the macrophage response triggered by stressed beta cells","authors":"Tina Zenia Jørgensen ,&nbsp;Knud Josefsen ,&nbsp;Signe Stentoft Dissing ,&nbsp;Karsten Buschard ,&nbsp;Julie Christine Antvorskov ,&nbsp;Jesper Larsen","doi":"10.1016/j.cellimm.2025.104989","DOIUrl":"10.1016/j.cellimm.2025.104989","url":null,"abstract":"<div><div>In humans, a gluten-free diet can slow disease progression and improve clinical outcome in newly diagnosed type 1 diabetes patients. In NOD mice, the incidence of autoimmune diabetes is influenced by both beta cell activity and gluten. Here, we demonstrate that metabolically stressed pancreatic cell lines (MIN6, beta TC3, and alpha TC3) effectively activated macrophage RAW 264.7 cells. Gliadin further enhanced this response in MIN6 cells but had no such effect on beta TC3 or alpha TC3 cells. Additionally, gliadin directly stimulated MIN6 cells, affecting pathways related to cellular activation, stress responses, and immune regulation. These findings provide insights into the in vivo benefits of a gluten-free diet in type 1 diabetes development by highlighting the roles of cellular stress and gliadin in disease progression.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"414 ","pages":"Article 104989"},"PeriodicalIF":3.7,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144280705","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":"Macrophage heterogeneity in autoimmune diseases","authors":"Shuaiyi Li,&nbsp;Xiaohui Zhou,&nbsp;Shidi Yu,&nbsp;Zenghui Liu,&nbsp;Mingshuang Sun,&nbsp;Zihou Si,&nbsp;Wei Zhu","doi":"10.1016/j.cellimm.2025.104993","DOIUrl":"10.1016/j.cellimm.2025.104993","url":null,"abstract":"<div><div>The pathogenesis of autoimmune diseases (AIDs) is complex and their etiology remains unclear, with multiple cell types involved in the disease progression. Macrophages, as a crucial immune cell population in AIDs, play a pivotal role in maintaining immune homeostasis. In traditional research, macrophages are frequently oversimplified into the M1 and M2 polarized subtypes. The advent of single-cell RNA sequencing (scRNA-seq) technology has significantly advanced high-throughput research in the life sciences, enabling in-depth investigations at the cellular and molecular levels. This technology has revealed the significant heterogeneity of macrophages, further enhancing our understanding of their development, phenotypic diversity, and functional plasticity. Additionally, it provides a novel perspective for exploring the molecular mechanisms underlying various diseases. In this review, we comprehensively explore the heterogeneity of macrophages across different AIDs, and summarize potential therapeutic targets for macrophage-directed interventions, aiming to provide valuable theoretical insights and novel research directions to advance precision therapy and related studies in AIDs.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"414 ","pages":"Article 104993"},"PeriodicalIF":3.7,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144280814","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":"Corrigendum to “Modular activation of macrophage-like cells by beta-2-microglobulin via mitochondria and the cGAS-STING pathway” [Cell. Immunol. 413 (2025) 104962]","authors":"Josefine Kofoed Corneliussen ,&nbsp;Helena Borland Madsen ,&nbsp;Nadia Thaulov Zelander ,&nbsp;Mogens Holst Nissen ,&nbsp;Claus Desler","doi":"10.1016/j.cellimm.2025.104984","DOIUrl":"10.1016/j.cellimm.2025.104984","url":null,"abstract":"","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"414 ","pages":"Article 104984"},"PeriodicalIF":3.7,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246663","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":"Aerobic exercise activates let-7e-5p through TP73-AS1 to inhibit the HMGB1/RAGE axis and alleviate asthma airway inflammation and remodeling","authors":"Dan Wang ,&nbsp;Jing Zhao ,&nbsp;Chunyan Yang ,&nbsp;Daogang Qin ,&nbsp;Dengna Zhu","doi":"10.1016/j.cellimm.2025.104990","DOIUrl":"10.1016/j.cellimm.2025.104990","url":null,"abstract":"<div><div>The rising incidence of asthma, a chronic respiratory condition, has been associated with the involvement of microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) in its pathogenesis. Nevertheless, there is a shortage of data pertaining to the impact of lncRNA TP73-AS1 and let-7e-5p on this disease. Therefore, we aimed to explore the possible effects of aerobic exercise (AE) on lncRNA TP73-AS1, let-7e-5p, inflammation, and high mobility group box 1 (HMGB1)/receptor for advanced glycation end products (RAGE) in asthma mouse models. HMGB1/RAGE was significantly upregulated in asthma mouse models using ovalbumin (OVA) stimulation. The overexpression of let-7e-5p, which was found to be significantly downregulated in asthma mouse models, appeared to inhibit EMT and might alleviate airway inflammation in asthmatic mice through the suppression of the HMGB1/RAGE pathway. Aerobic exercise was associated with reduced airway inflammation and remodeling in asthmatic mice, and appeared to suppress TP73-AS1 expression in asthma OVA-mouse models. Furthermore, TP73-AS1 may exacerbate airway inflammation and remodeling in OVA-induced asthmatic mice by downregulating let-7e-5p expression, which could activate the HMGB1/RAGE-NF-κB pathway. These findings suggest potential innovative approaches for asthma management, which warrant further validation.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"414 ","pages":"Article 104990"},"PeriodicalIF":3.7,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144240096","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 approach to hematopoietic stem cell transplantation: The effect of CMV infection and HLA genotypes on chimerism status in Egyptian patients","authors":"Raghda Mohammed Ghorab ,&nbsp;Hala Ahmed Talkhan ,&nbsp;Asmaa Mohamed Abd ElGwad ,&nbsp;Rania AbdelMoniem Radwan ,&nbsp;Hoda Ezz Elarab Abdelwahab ,&nbsp;Doaa Mohamed Abd El Aziz","doi":"10.1016/j.cellimm.2025.104991","DOIUrl":"10.1016/j.cellimm.2025.104991","url":null,"abstract":"<div><div>Several studies have investigated the association between HLA alleles and cytomegalovirus (CMV) infection following hematopoietic stem cell transplantation (HSCT). It was found that many HLA alleles were associated with increased rate of CMV infection, while others had a protective effect against infection. However, to our knowledge no studies have investigated the effect of this relation on chimerism status post transplantation. Previous results concluded that CMV reactivation or infection increases conversion from mixed chimerism toward complete chimerism (CC) as a consequence of concomitant activation of immune system. Our aim is to study the association of CMV and certain HLA alleles and their effect on chimerism status post transplantation and identify other factors affecting chimerism status. 165 patients who underwent allogeneic HSCT for different hematological indications were studied. Both recipients (R) and donors (D) underwent serological testing for CMV-specific IgG and IgM, HLA typing, and chimerism analysis. CMV infection or reactivation was assessed in recipients through weekly monitoring of CMV DNA. Patients were followed up for 100 days where chimerism analysis was performed at 28, 60, 90, and 100 days post-transplantation. Eighty-five patients were positive for CMV by PCR post transplantation while eighty patients were CMV negative. Acute graft versus host disease (aGvHD) was significantly increased in CMV positive patients. Multivariate analysis (MVA) has indicated that HLA-A*2, HLA-B*14, HLA-B*41, HLA-DRB1*04 and HLA-DRB1*13, as well as a diagnosis of myelodysplastic syndrome and bone marrow aplasia, significantly increased the risk for CMV positivity post transplantation. HLA-DRB1*11 positivity was associated with a higher rate of aGvHD. CMV infection/reactivation as indicated by positive CMV PCR post-transplant was associated with a faster rate of conversion toward CC, and this effect was independent of the implemented conditioning regimen or the presence of aGvHD. Additionally, D+/R- transplant setting was significantly associated with early CC. On MVA, CMV reactivation was associated with acceleration of conversion toward CC, while HLA-A*33, HLA-DRB1*13, HLA-DRB1*15 and D−/R+ transplant setting were factors associated with delayed CC. In conclusion, CMV infection/reactivation and D+/R- transplant setting were associated with earlier conversion toward CC. Chronic GvHD and early chimerism were associated with better overall survival (OS), while advanced recipient age and HLA-DRB1*01 were associated with lower OS.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"414 ","pages":"Article 104991"},"PeriodicalIF":3.7,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144280704","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":"“Mesenchymal stem cell-derived exosomes (MSC-exosomes) in hematology: From mechanisms to clinical breakthroughs”","authors":"Irfan Ahmad ,&nbsp;Ahmed Hussein ,&nbsp;Bhavesh Kanabar ,&nbsp;Abhinav Kumar ,&nbsp;T. Ramachandran ,&nbsp;Aman Shankhyan ,&nbsp;A. Karthikeyan ,&nbsp;Dhirendra Nath Thatoi ,&nbsp;Zafar Aminov ,&nbsp;Hamed Soleimani Samarkhazan ,&nbsp;Zahra Jafari","doi":"10.1016/j.cellimm.2025.104986","DOIUrl":"10.1016/j.cellimm.2025.104986","url":null,"abstract":"<div><div>Mesenchymal stem cells (MSCs) offer promising therapy because they regulate the immune system and help repair tissues. However, challenges such as low cell survival rates, immune rejection, and ethical concerns related to their clinical use have limited their widespread application. To overcome these limitations, MSC-derived exosomes (MSC-EXOs) have emerged as an innovative and promising cell-free therapeutic strategy. MSC-EXOs are nanosized extracellular vesicles released by MSCs that carry a diverse array of bioactive molecules, including proteins, lipids, and nucleic acids. They share many benefits with MSCs, including immune regulation, anti-inflammatory effects, and tissue repair. MSC-EXOs demonstrate therapeutic potential by modulating the tumor microenvironment, suppressing tumor growth, and enhancing the efficacy of conventional therapies. They can specifically target cells, deliver therapeutic agents, and induce apoptosis in cancer cells. Additionally, MSC-EXOs can modulate the immune response, promote hematopoietic recovery, and alleviate treatment-related side effects. While MSC-EXOs present a promising therapeutic approach, several challenges remain, including the standardization of isolation and characterization methods, understanding their mechanisms of action, and ensuring both safety and efficacy. Despite these challenges, the future of MSC-EXO-based therapies in hematology is promising. Continued research efforts are essential to unravel the intricate biology of exosomes, identify novel biomarkers, and develop innovative therapeutic strategies. By harnessing the power of MSC-EXOs, we can revolutionize the treatment of hematological diseases and improve patient outcomes.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"414 ","pages":"Article 104986"},"PeriodicalIF":3.7,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144240103","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":"Retraction notice to \"Protective efficacy of a plasmid DNA vaccine against transgene-specific tumors by Th1 cellular immune responses after intradermal injection\" [Cell. Immunol. 329 (2018) 17–26]","authors":"Hye-Youn Son ,&nbsp;Vasso Apostolopoulos ,&nbsp;June-Key Chung ,&nbsp;Chul-Woo Kim ,&nbsp;Ji-Ung Park","doi":"10.1016/j.cellimm.2025.104975","DOIUrl":"10.1016/j.cellimm.2025.104975","url":null,"abstract":"","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"413 ","pages":"Article 104975"},"PeriodicalIF":3.7,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144186607","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}