细胞与分子免疫学杂志最新文献

{"title":"[The mechanism and research progress of vitamin A in the prevention and treatment of atopic dermatitis in children].","authors":"Min Wang, Han Zhou, Yue Qin, Yun Zhang, Xuehua Zhou, Hong Tan, Huajie Wu, Xin Sun","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Atopic dermatitis (AD) is a chronic, recurrent, inflammatory, and pruritic skin disease associated with genetic predisposition to allergies. As one of the most common chronic allergic diseases in children, the global incidence of AD has been on the rise in recent years, imposing a significant burden on the quality of life of affected children and the economic status of their families. Vitamin A, as an essential fat-soluble vitamin, not only participates in the visual cycle and maintains epithelial homeostasis but also plays a crucial role in the immune regulation of allergic diseases such as AD. Vitamin A deficiency exacerbates the progression of AD by enhancing type 2 helper T (Th2)-mediated inflammatory responses and mast cell activation, whereas exogenous vitamin A supplementation exerts a protective effect in the early stage of the disease. Vitamin A and its metabolites exert anti-inflammatory effects through multiple mechanisms: regulating mast cell; remodeling natural killer (NK) cell; inducing T cell differentiation; modulating the differentiation and function of innate lymphoid cell (ILC) and regulating the gut microbiota. In summary, vitamin A participates in AD-related immune regulation through multiple pathways, holding significant basic research value and promising clinical application prospects. This review will systematically summarize the role of vitamin A in the pathogenesis of AD and its potential therapeutic value.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 4","pages":"367-372"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147790426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[MiR-21 targets PDCD4 to regulate proliferation, apoptosis, and invasion of osteosarcoma MG63 cells].","authors":"Zhipeng Wang, Ziru Zhang, Jian Zhao","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective MicroRNAs (miRNAs) are small endogenous single-stranded non-coding RNAs, approximately 20-25 nucleotides in length, that regulate the expression of potential target mRNAs at the post-transcriptional level. miRNAs are abnormally expressed in many malignant tumors, and are closely associated with tumorigenesis and development, functioning either as proto-oncogenes or oncogenes. Studies have revealed that microRNA-21 (miR-21) is one of the most common oncogenes across various cancer types. However, the function of miR-21 in osteosarcoma has not been fully elucidated. This study aims to investigate the effect of miR-21 on the proliferation, invasion and apoptosis of osteosarcoma cell line MG63 and its underlying mechanisms. Methods Bioinformatics was used to predict the potential target genes of miR-21. The expression levels of miR-21 and programmed cell death 4 (PDCD4) in osteosarcoma cell line MG63 were measured by qRT-PCR and Western blot, respectively. After the expression of miR-21 was regulated (either up-regulated or inhibited), its biological effects on cell viability, cell cycle progression and apoptosis were assessed. The targeting relationship between miR-21 and PDCD4 was verified by using dual-luciferase reporter gene assay. Results Bioinformatics prediction showed that the 3'-UTR region of human PDCD4 gene contained multiple potential miRNA target sites. qRT-PCR results showed that the expression level of miR-21 in the pcDNA3.1-miR-21 group was significantly higher than that in the pcDNA3.1 group and the blank group. Compared with the blank group, up-regulation of miR-21 significantly promoted the proliferation and invasion of osteosarcoma MG63 cells, while inhibiting cell apoptosis. Luciferase reporter gene assay confirmed that PDCD4 was a direct target gene of miR-21, and there was a negative correlation between miR-21 and PDCD4. Conclusion Up-regulation of miR-21 expression promotes proliferation and invasion while inhibiting apoptosis of osteosarcoma cell line MG63 by suppressing the level of endogenous PDCD4. In contrast, down-regulation of miR-21 expression inhibits proliferation and invasion while promoting apoptosis of osteosarcoma cell line MG63. Therefore, miR-21 functions as an oncogene in the development of osteosarcoma and could be a potential therapeutic target.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 4","pages":"307-315"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147790384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Association between anemia and rheumatoid arthritis: a cross-sectional and Mendelian randomization study].","authors":"Yanwen Liu, Yingming Xu, Youqun Zhang, Xinyi Wang, Junfeng Jia, Zhaohui Zheng, Kui Zhang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective To investigate the correlation between anemia and rheumatoid arthritis (RA), and to analyze the potential impact and causal relationship between them. Methods Using data from the National Health and Nutrition Examination Survey (NHANES) database, a logistic regression model was constructed to assess the association between anemia and RA; subgroup analysis was performed to verify the stability of the results. Subsequently, a two-sample mendelian randomization (MR) analysis was conducted to explore the bidirectional causal relationship between anemia and RA. Results Multivariate logistic regression analysis revealed a positive correlation between anemia and RA (OR=1.21, 95%CI: 1.05-1.40), and subgroup analysis further confirmed the stability of these results. Furthermore, MR analysis indicated a bidirectional causal relationship between anemia and RA, with no observed evidence of horizontal pleiotropy or heterogeneity. Conclusion Anemia and RA demonstrate a significant correlation and a bidirectional causal relationship at multiple levels.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 4","pages":"325-331"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147790412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Research progress on the role of MST1 kinase in mast cell-mediated hypersensitivity reactions].","authors":"Bayina Batesurong, Jianrong Ye","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Hypersensitivity reactions refer to immune responses characterized by an increased sensitivity upon re-exposure to the same antigen after initial sensitization. Among them, the hypersensitivity reaction mediated by immunoglobulin E (IgE) and mast cells is classified as type I hypersensitivity. Mast cells, which are widely distributed in the connective tissues and mucosal layers of various organs throughout the body, serve as key effector cells in type I hypersensitivity reactions. During this process, when mast cells encounter specific allergenic proteins again, IgE molecules bound to their surface cross-link with the allergens, triggering cell activation and degranulation. This leads to the release of histamine, cytokines, chemokines, as well as newly synthesized arachidonic acid metabolites and various proteins that regulate the type I hypersensitivity response. Macrophage stimulating factor 1 (MST1) plays multiple crucial roles in cellular biology, including the regulation of cell migration, apoptosis, proliferation, metabolism, and cytoskeletal dynamics. This review focuses on the regulatory mechanisms of MST1 kinase and its influence on type I hypersensitivity, aiming to provide new insights into the mechanisms and prevention strategies of allergic diseases.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 4","pages":"348-353"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147790450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Research progress on the role of macrophage efferocytosis in chronic obstructive pulmonary disease].","authors":"Shumin Feng, Tao Bian","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Lung macrophages (LM), as pivotal immune effector cells in the pulmonary system, possess the capacity to clear apoptotic cells through a process termed efferocytosis. Efferocytosis represents a tightly regulated biological process involving multiple sequential steps including recognition, binding, engulfment, and digestion of apoptotic cells by LM, playing a crucial role in maintaining pulmonary homeostasis and modulating inflammatory responses. Evidence demonstrates that efferocytosis by LM is impaired in patients with chronic obstructive pulmonary disease (COPD), and this dysfunction is closely associated with the chronic inflammation, tissue remodeling, and disease progression in COPD. This review focuses on the efferocytosis of LM as a therapeutic target to provide in-depth exploration of the molecular mechanisms underlying efferocytic dysfunction in COPD and the potential intervention strategies, with the aim of offering novel insights for COPD prevention and treatment.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 4","pages":"361-366"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147790379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Molecular mechanisms of mitochondrial dysfunction mediated by the MAPK axis in diabetic cataract].","authors":"Yanxi Wang, Yingying Heng, Yan Xu, Yalan Chen, Mengyi Lin, Guiqu Wang, Gangjin Kang, Siquan Zhu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective To explore molecular mechanisms of mitochondrial dysfunction mediated by p38 mitogen-activated protein kinase (p38 MAPK) in diabetic cataract (DC). Methods Lens epithelial cells (LECs) from cell line SRA01/04 were divided into the following six treatment groups: blank group (Con), osmotic control group, high glucose group (HG), HG+sh-p38 MAPK group, HG+sh-p38 MAPK+oe-NC group and HG+sh-p38 MAPK+oe-Pink1 group. The Con group was exposed to normal glucose concentration (5.5 mmol/L) for 48 hours; the osmotic control group was exposed to 5.5 mmol/L glucose and 49.5 mmol/L mannitol for 48 hours; the other groups were exposed to 55 mmol/L glucose for 48 hours to induce a DC model in vitro. 36 Sprague-Dawley rats were divided into a control group, a DC group and a DC+SB203580 group, with 12 rats in each group. At the 12th week, the lens of each group were analyzed histologically. Oxidative stress indicators like malondialdehyde (MDA), reactive oxygen species (ROS), superoxide dismutase (SOD), ATP synthase activity, mitochondrial membrane potential analysis, and mitochondrial DNA (mtDNA) copy number were measured using commercial kits. The protein expression was analyzed using Western blot. Results Compared with the Con group, the HG group showed significantly increased levels of MDA and ROS, but significantly decreased levels of SOD, ATP synthase activity, mtDNA copy number and the JC-1 red/green (aggregate/monomer) ratio in LECs. Compared with the HG group, the HG+sh-p38 MAPK group exhibited significantly decreased levels of MDA and ROS, but significantly increased levels of SOD, ATP synthase activity, mtDNA copy number and the JC-1 red/green (aggregate/monomer) ratio in LECs. Compared with the HG+sh-p38 MAPK group, the HG+sh-p38 MAPK+oe-Pink1 group showed significantly decreased ATP synthase activity, mtDNA copy number and JC-1 red/green ratio in LECs. In LECs of HG+sh-p38 MAPK+oe-Pink1 group, the protein levels of PTEN-induced kinase 1 (Pink1), Parkin, microtubule-associated protein 1 light chain 3 (LC3) II/LC3 I, cleaved caspase-3 (c-caspase-3) and Cytochrome C (Cyt-C) were higher than those of HG+sh-p38 MAPK group, while the protein levels of p62 and B cell lymphoma 2 (Bcl2) were lower. The expression of p-p38 MAPK in LECs of rats in DC+SB203580 group was lower than that in DC group. Compared with the control group, the DC group exhibited significantly increased levels of ROS and MDA and the expression levels of mitochondrial autophagy-related proteins (including Parkin, Pink1, LC3-II/LC3-I ratio, c-caspase-3 and Cyt-C), but significantly decreased levels of SOD, p62 and Bcl2 proteins. SB203580 treatment showed the opposite regulatory effect. Conclusions In both in vitro and in vivo DC models, inhibition of p38 MAPK signaling down-regulates the Pink1/Parkin pathway, thereby reducing the oxidative stress caused by LEC mitochondrial dysfunction and attenuating the histopathological changes in the lens of DC rats.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 4","pages":"316-324"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147790404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Research progress on the Co-Presentation of CD8⁺ T cell antigen epitopes by HLA-A*02 and HLA-E in infectious diseases].","authors":"Jiajia Zuo, Xiaoyue Xu, Kexuan Zhao, Yusi Zhang, Chunmei Zhang, Yun Zhang, Lihua Chen, Xiaobin Liu, Ying Ma","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Human leukocyte antigen (HLA) plays a pivotal role in immune responses. As a classical HLA-Ia among the HLA molecules, HLA-A*02 activates CD8⁺ T cells by presenting endogenous antigenic peptides, thereby contributing significantly to antiviral immunity. In contrast, the non-classical HLA-Ib molecule HLA-E regulates immune homeostasis through interactions with the CD94/NKG2 receptor expressed on natural killer (NK) cells. Recent studies have revealed that HLA-E could also present pathogen or tumor-derived antigenic peptides to activate specific CD8⁺ T cells. Notably, the peptide sequences presented by HLA-E exhibit high similarity to those presented by HLA-A*02, suggesting potential cooperative or competitive mechanisms underlying their involvement in CD8⁺ T cell-mediated anti-pathogen immune responses. This review systematically compares the structural and functional bases of antigen presentation mechanisms, particularly focusing on their shared capacity to present pathogen-derived epitopes during infectious diseases for HLA-A*02 and HLA-E. We further discussed the roles of their co-presentation phenomenon in host defense and immune homeostasis maintenance. The design of novel peptide vaccines based on the co-presentation of antigenic epitopes by HLA-A*02 and HLA-E may overcome limitations posed by HLA polymorphism, offering a theoretical basis and novel strategies for achieving broader and longer-lasting immune protection.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 4","pages":"354-360"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147790391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Inhibitory effect and mechanism of low-intensity ultrasound combined with 5-fluorouracil on human hepatocellular carcinoma HepG2 cells].","authors":"Yi Lu, Weihan Zhang, Fuyu Yang, Limin Jia, Hefei Wang, Qiyan Guan, Zizhan He, Mei Liu, Yanhong Lyu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective To investigate the cytotoxic effects and underlying mechanisms of 5-fluorouracil (5-FU) combined with low-intensity ultrasound (LIUS) in human hepatocellular carcinoma HepG2 cells. Methods HepG2 cells were treated with LIUS (1.0 MHz, 0.5 W/cm², duty cycle 20%) in combination with 5-FU. Intracellular 5-FU accumulation was quantified using a fluorescence microplate reader. Cell viability was assessed using an MTT assay, and apoptosis was measured by Annexin V/PI staining followed by flow cytometry. Membrane fluidity was assessed by fluorescence polarization. The expression levels of equilibrative nucleoside transporter 1 (ENT-1) and P-glycoprotein (P-gp) were detected by Western blot and immunofluorescence. Immunofluorescence staining was further used to evaluate the expression and translocation of immunogenic cell death (ICD) markers, calreticulin (CRT), and high mobility group protein B1 (HMGB1). Results LIUS significantly enhanced the intracellular accumulation of 5-FU in HepG2 cells. Compared with untreated cells or those treated with 5-FU alone, the combination of LIUS and 5-FU significantly reduced cell viability and increased early and total apoptosis. Membrane fluidity was significantly increased in the combination group. Additionally, the expression of ENT-1, which mediated drug influx, was significantly upregulated, while the expression of the drug efflux protein P-gp was markedly downregulated. CRT translocated to the cell surface, and HMGB1 was released from the nucleus to the cytoplasm and extracellular space, indicating the induction of ICD. Conclusion LIUS enhances the intracellular accumulation of 5-FU in HepG2 cells. The combination of 5-FU and LIUS exerts potent cytotoxic effects by upregulating ENT-1 and downregulating P-gp, and induces immunogenic cell death in hepatocellular carcinoma cells.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 4","pages":"299-306"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147790365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[A study on the effect of aqueous extract of Euphorbia helioscopia on improving immune environment and inhibiting the formation of pulmonary tumor nodules].","authors":"Xuhui Jin, Wenbin Duan, Lanying Chen, Yuqing Huang, Yajuan Chen, Ronghua Liu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective To explore the effect and mechanism of aqueous extract of Euphorbia helioscopia L. (EHE) on improving the immune environment and inhibiting lung tumor nodules induced by lipopolysaccharide (LPS) combined with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in mice. Methods Male BALB/c mice were randomly divided into 6 groups: normal group, model group, Euphorbia helioscopia water extract low-, medium-, and high-dose groups (0.9, 1.8, 3.6 g/kg), and aspirin group (20 mg/kg). Samples were collected after 25 weeks. HE and immunohistochemistry staining were used to detect tumor lesions in lung tissues. Western blot was performed to determine the expression of oncoproteins in lung tissues. Real-time fluorescence quantitative PCR and flow cytometry were employed to detect the mRNA levels of immune-related molecule genes and the percentage of immune cells in lung tissues, respectively. Additionally, Western blot was used to detect the expression of proteins related to immune regulatory pathways. Results HE and immunohistochemistry staining revealed that LPS combined with NNK induced the formation of adenomatous tumor nodules in mice, with high expression of thyroid transcription factor 1 (TTF-1) in the lungs. Compared with the model group, the Euphorbia helioscopia-treated groups exhibited a significant reduction in the number of lung tumor nodules, decreased expression of the oncoprotein c-Myc and anti-apoptotic protein Bcl2, and increased expression of the pro-apoptotic protein BAX. The mRNA levels of immune-related molecules in lung tissues, including S100 calcium-binding protein A9 (S100A9), cyclooxygenase 2 (COX2), granulocyte-macrophage colony-stimulating factor (GM-CSF), chemokine ligand 1 (CXCL1), monocyte chemoattractant protein 1 (MCP-1), interleukin 10 (IL-10), and IL-4, were significantly downregulated. In lung tissues, the percentage of macrophages increased, while the percentage of myeloid-derived suppressor cells (MDSCs) decreased. In the spleen, the percentages of regulatory T cells (Tregs) and MDSCs were reduced. The protein expression levels of programmed death ligand 1 (PD-L1), cluster of differentiation 47 (CD47), phosphorylated nuclear factor κB p65 subunit (p-NF-κB p65), and phosphorylated signal transducer and activator of transcription 3 (p-STAT3) were decreased. Conclusion The aqueous extract of Euphorbia helioscopia L. can effectively inhibit LPS/NNK-induced formation of lung adenoma nodules by improving the immune environment, and its mechanism may involve regulating the activation of NF-κB and STAT3.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 4","pages":"289-298"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147790421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Regulation of immune cell function by the unfolded protein response and its underlying mechanisms].","authors":"Jiyang Zheng, Yazhen Wang, Ziye Hui, Yingjun Peng, Qi Peng, Yue Luo, Lihua Chen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The unfolded protein response (UPR) serves as a pivotal regulatory mechanism that enables cells to mitigate endoplasmic reticulum proteostasis disturbance. The evolutionarily conserved pathway encompasses three core signalings, namely the inositol-requiring enzyme 1α-X-Box-protein-1s (IRE1α-XBP1s), protein kinase RNA-like endoplasmic reticulum kinase-eukaryotic initiation factor-2α-activating transcription factor 4 (PERK-eIF2α-ATF4), and activating transcription factor 6 (ATF6) pathways. Notably, the activation of UPR pathway modulates the phenotype and functional properties of immune cells, and is intricately involved in the pathogenesis and progression of diverse immune-related disorders. In this review, we provide a systematic overview of the molecular mechanisms underlying UPR activation in different immune cell subsets, and further delve into the regulatory roles of UPR signaling in the survival, development, differentiation, and effector functions of immune cells. Collectively, this review aims to provide a theoretical framework for comprehensively elucidating the pivotal roles of UPR in immune responses and the pathogenesis of immune-related diseases.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 4","pages":"339-347"},"PeriodicalIF":0.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147790445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}