细胞与分子免疫学杂志最新文献

{"title":"[The distribution of high-resolution alleles and haplotypes of HLA-A, -B, -C, -DRB1, and -DQB1 in the Han population of Shandong Province].","authors":"Jingru Shao, Hua Shen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective This study aims to investigate the polymorphism and distribution characteristics of high-resolution HLA-A, -B, -C, -DRB1, and -DQB1 alleles and haplotypes in the Han population from Shandong province. Methods High-resolution genotyping of HLA-A, -B, -C, -DRB1, and -DQB1 loci was performed on 8618 samples using the PCR-SBT method. Allele frequencies and haplotypes were analyzed with Arlequin 3.5 software, phylogenetic analysis was conducted using Mega 6.0, and multidimensional scaling analysis was performed with SPSS 21.0. Results In this study, the number of distinct alleles detected among the 8618 samples was as follows: 53 HLA-A alleles, 108 HLA-B alleles, 67 HLA-C alleles, 53 HLA-DRB1 alleles, and 25 HLA-DQB1 alleles, including 24 rare alleles. The most common alleles at the HLA-A, -B, -C, -DRB1, and -DQB1 loci were A*02:01, B*13:02, C*06:02, DRB1*15:01, and DQB1*03:01, respectively. A total of 4957 HLA-A-B-C-DRB1-DQB1 haplotypes were detected, among which five had a frequency greater than 1%. The most common haplotype was A*30:01-B*13:02-C*06:02-DRB1*07:01-DQB1*02:01. Phylogenetic analysis showed that the Shandong Han population clustered together with the Northern Han population, and the multidimensional scaling analysis yielded results consistent with the phylogenetic analysis. Conclusion This study provides relatively comprehensive high-resolution distribution data of HLA-A, -B, -C, -DRB1, and -DQB1 alleles and haplotypes in the Shandong Han population, enriching the HLA polymorphism data for this region. More importantly, for the first time based on a large sample, this study reveals the distribution characteristics of high-resolution HLA-A, -B, -C, -DRB1, and -DQB1 alleles and haplotypes in the Shandong Han population, filling the gap in high-quality HLA genetic data for this region. These findings provide an important basis for optimizing hematopoietic stem cell donor registries, developing transplantation matching strategies, and conducting disease association studies.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 10","pages":"917-924"},"PeriodicalIF":0.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149139516","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":"[Identification of immune key genes in sepsis and the regulatory effects of dexmedetomidine based on transcriptome analysis and machine learning].","authors":"Xiaofeng Chen, Mingdi Chen, Fujun Li, Meifeng Chen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective This study aims to identify immune-related key genes in sepsis using transcriptomic analysis and machine learning, and to explore the role of dexmedetomidine (DEX) in sepsis regulation through these genes. Methods The transcriptomic dataset GSE9960 related to sepsis was obtained from the gene expression omnibus (GEO) database. Differential expression analysis and visualization were performed using the limma and ggplot2 packages in R 4.5.1. DEX targets were collected from the comparative toxicogenomics database (CTD), SwissTargetPrediction, and GeneCards databases, followed by integration and removal of duplicates to obtain the overall DEX target set. Immune-related targets were also retrieved from the GeneCards database. The DEX targets, sepsis-related targets, and immune-related targets were intersected to identify DEX-targeted immune-related sepsis targets. Key targets were screened using least absolute shrinkage and selection operator (LASSO) regression and random forest (RF) algorithms, and the overlapping targets were further identified as core DEX-targeted immune targets in sepsis. Immune infiltration was evaluated using the CIBERSORT algorithm combined with Spearman correlation analysis, and the correlations between core targets and immune cell populations were further investigated. In vitro, a sepsis cell model was established by lipopolysaccharide (LPS) stimulation of the human monocyte cell line THP-1. Target gene knockdown or overexpression was achieved through gene transfection. Western blot analysis was performed to evaluate the effects of DEX treatment and potassium calcium-activated channel subfamily M α1 (KCNMA1) regulation on sepsis-related proteins and inflammatory cytokine levels. Results Sepsis-related dataset GSE9960 exhibited significant differential expression. After integrating and removing duplicates among sepsis-, immune-, and DEX-related targets, 25 key immune targets of DEX against sepsis were identified. LASSO and RF analyses further screened three core targets. Immune infiltration analysis showed that these core targets were significantly associated with plasma cells, neutrophils, and resting memory CD4⁺ T cells. Since KCNMA1 exhibited the most prominent upregulation and the greatest differential expression, it was selected for further experimental validation. The results demonstrated that DEX treatment reduced the expression of sepsis-related proteins, including KCNMA1, cyclin B2 (CCNB2), and NEDD4 E3 ubiquitin protein ligase (NEDD4), and suppressed inflammatory cytokine levels by downregulating KCNMA1. Conclusion DEX suppresses the development of sepsis by downregulating KCNMA1 expression.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 9","pages":"777-785"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148984185","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 and application status of nanobody-drug conjugate(NDC) in cancer treatment].","authors":"Gelin Xian, Yingjiao Li, Mengyuan Hu, Fei Yan","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Nanobody (Nb) is a unique type of single-domain antibody found in camelids, comprising only the variable domain of heavy-chain-only antibodies (VHH). Nbs prossess distinct advantages, including small molecular size, high structural stability, high solubility, strong antigen-binding affinity, and low. While, antibody-drug conjugates (ADCs) have shown significant efficacy in cancer therapy, conventional ADCs based on monoclonal antibodies face limitations such as poor tissue penetration, high immunogenicity and immunotoxicity, and costly production. Studies suggested that replacing monoclonal antibodies with Nbs to construct nanobody-drug conjugates (NDCs) can circumvent these drawbacks. By conjugating Nbs with chemotherapeutic drugs, photosensitizers, or radionuclides, and other agents, NDCs enhance therapeutic effect and demonstrate great potential in tumor diagnosis and treatment. This review summarizes the discovery and structural characteristics of nanobodies, the construction strategies for NDCs, their applications in tumor therapy, and the synergistic potential of nanobodies with other treatment modalities. Ultimately, it aims to provide insights for future research and development of NDCs in oncology.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 9","pages":"827-836"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148984250","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":"[Advances in the mechanistic researches of neutrophil extracellular trap in pulmonary diseases].","authors":"Zhiliang Fan, Yihui Chai, Qian Li, Yunzhi Chen, Zengjie Gao, Tingwei Shi, Jianjun Niu, Xiang Pu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Neutrophil extracellular trap (NET), as an important effector mechanism of innate immunity, plays a critical regulatory role in various pulmonary diseases, including coronavirus disease-associated acute respiratory distress syndrome, bacterial pneumonia, sepsis, pulmonary fibrosis (PF), and chronic obstructive pulmonary disease. NET can be released by activated neutrophils through multiple mechanisms. Among them, classical suicidal NETosis represents one of the major pathways and contributes substantially to host defense against infection. However, the excessive accumulation of NET can lead to tissue damage, immunothrombosis, and chronic inflammation. By amplifying inflammatory cascades, disrupting tissue homeostasis, and triggering immunothrombotic processes, aberrant NET formation can also promote the development and progression of lung diseases. This review systematically summarizes the mechanisms of NET formation, metabolic regulation, autophagy, and their interactions with platelets. It provides an in-depth discussion of the roles and clinical significance of NET in both acute and chronic pulmonary diseases. Furthermore, potential therapeutic strategies targeting NET are highlighted. These strategies aim to offer new theoretical foundations and interventional perspectives for the prevention and treatment of pulmonary diseases.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 9","pages":"837-843"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148984277","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":"[Knockdown of IL-1R8 augments the tumor-suppressive capacity of ex vivo expanded natural killer (NK) cells against hepatocellular carcinoma].","authors":"Jiangling Song, Qingqing Zuo, Shengjie Zhang, Min Yu, Jianfeng Li, Longzi Liu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective Interleukin-1 receptor 8 (IL-1R8) is significantly upregulated in activated natural killer (NK) cells and serves as a critical negative regulator governing the anti-tumor immune activity of NK cells. This study aims to silence IL-1R8 expression in ex vivo expanded NK cells, and further elucidate the underlying molecular mechanism by which IL-1R8 modulates NK cell-mediated anti-tumor immunity against hepatocellular carcinoma (HCC). Methods IL-1R8 expression was knocked down in ex vivo expanded NK cells using lentivirus-derived IL-1R8 short hairpin RNA (shRNA), and the knockdown efficiency was verified by real-time quantitative PCR (qPCR) and Western blotting. Trypan blue staining was used to assess NK cell proliferation, while flow cytometry analyzed changes in the expression of major phenotypic receptors before and after IL-1R8 knockdown. A lactic dehydrogenase (LDH) release assay evaluated the in vitro cytotoxicity of NK cells against HCC cells, and ELISA measured the secretion levels of cytokines and chemokines during the killing process. A Huh7 xenograft mouse model was established to verify the in vivo anti-tumor therapeutic efficacy of IL-1R8-silenced NK cells. Immunohistochemical staining was performed to detect the intratumoral levels of NK cells within tumor tissues. Results Knockdown of IL-1R8 exerted no significant effects on the proliferation capacity and surface phenotypic characteristics of ex vivo expanded NK cells. Nevertheless, IL-1R8 downregulation remarkably potentiated the cytotoxicity of NK cells against HCC, and facilitated the secretion of multiple core anti-tumor cytokines and chemokines, including tumor necrosis factor α (TNF-α), interferon γ (IFN-γ), C-C motif chemokine ligand 3 (CCL3) and C-X-C motif chemokine ligand 8 (CXCL8). In vivo animal experiments demonstrated that adoptive transfer of IL-1R8-knockdown NK cells significantly suppressed subcutaneous HCC tumor growth, meanwhile enhanced NK cell recruitment and infiltration in the tumor microenvironment. Conclusion Genetic ablation of IL-1R8 efficiently augments the anti-tumor effector function of NK cells against HCC both in vitro and in vivo, highlighting IL-1R8 as a promising target to improve the efficacy of NK cell-based therapies for cancer treatment.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 9","pages":"769-776"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148984216","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":"[Production and application of rabbit polyclonal antibody against ARRDC5].","authors":"Yaru Li, Linwei Xu, Lu Yuan, Yuxin Gao, Nuo Shen, Fan Yang, Ying Zheng, Changmin Niu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective To produce rabbit polyclonal antibody against arrestin domain-containing protein 5 (ARRDC5). Methods The recombinant prokaryotic plasmid pET-30a-Arrdc5 was constructed using molecular cloning techniques, introduced into E. coli BL21 (DE3), subsequently induced with isopropyl β-D-1-thiogalactopyranoside (IPTG) to express the recombinant ARRDC5 protein. After purification with Polyhistidine-tag (His-Tag) affinity column, New Zealand white rabbits were immunized with ARRDC5 protein. The antibody titer was assessed by ELISA. ARRDC5 protein expression in mouse testes was detected by Western blot. IP-MS was performed to identify the interacting proteins of ARRDC5 in the testis. Results The pET-30a-Arrdc5 recombinant plasmid was constructed correctly, and recombinant ARRDC5 protein was expressed and purified successfully by IPTG induction. After immunization, the titer of ARRDC5 antibody reached 1:512 000. The ARRDC5 protein was specifically recognized by ARRDC5 antibody in mouse testes. A total of 365 ARRDC5-interacting proteins were identified, which were significantly enriched in spermatogenesis-related biological processes. Co-IP results validated the interaction between ARRDC5 and pyruvate kinase isozyme M2 (PKM2). Conclusion The rabbit polyclonal antibody against ARRDC5 was generated successfully, which facilitates further investigation of ARRDC5 in spermatogenesis.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 9","pages":"813-817"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148984218","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":"[Transcriptomic analysis of NT5E/CD73-related macrophage state remodeling in the maternal-fetal immune microenvironment of recurrent pregnancy loss].","authors":"Heying Huang, Bing Liu","doi":"","DOIUrl":"","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Objective To investigate changes in the immune microenvironment of placental villous tissue in recurrent spontaneous abortion (RSA) based on transcriptomic analysis, and to preliminarily explore the potential relationship between the adenosine-NT5E/CD73 axis and macrophage state remodeling. Methods The placental villous tissue transcriptome dataset GSE237732, including RSA and normal pregnancy samples, was obtained from the gene expression omnibus (GEO) database. Candidate key genes were screened by differential expression analysis, weighted gene co-expression network analysis (WGCNA), and protein-protein interaction (PPI) network analysis. Immune infiltration analysis was performed to assess the association between key genes and relative immune cell abundance, and gene set enrichment analysis (GSEA) was used to explore related signaling pathways. The placental microarray dataset GSE22490 was used for independent validation of NT5E expression and macrophage/inflammation-related signatures. The decidual CD45&lt;sup&gt;+&lt;/sup&gt; immune cell single-cell dataset GSE164449 was also analyzed as an exploratory bypass dataset. Finally, a THP-1-derived macrophage model was used to evaluate the effects of CD73 inhibition and adenosine supplementation on inflammatory markers of M1 macrophages. Results Nine key genes were identified from GSE237732, including PDGFRB, DCN, COL6A1, COL5A2, PDGFRA, LTBP2, TIMP1, ENG, and NT5E. Immune infiltration analysis showed that all nine key genes were significantly correlated with M1 macrophages; ENG and NT5E were negatively correlated, whereas the other genes were positively correlated. GSEA indicated that NT5E was involved in multiple pathways related to immune dysregulation and inflammatory responses. In GSE22490, NT5E expression showed a decreasing trend in the recurrent miscarriage group, whereas CD86 and M1/inflammatory signatures showed increasing trends, although these changes were not statistically significant. The M2 macrophage signature was significantly increased, suggesting overall macrophage state remodeling rather than isolated M1 elevation. Exploratory single-cell analysis of GSE164449 showed increased macrophage-like cell proportions and increased M1- and M2-related scores in RPL-associated decidual CD45&lt;sup&gt;+&lt;/sup&gt; immune cells. Quantitative real-time PCR and flow cytometry showed that APCP-mediated inhibition of NT5E/CD73 activity increased inflammatory factor expression and the CD86&lt;sup&gt;-&lt;/sup&gt;positive rate in M1 macrophages, whereas adenosine supplementation partially reversed these effects. Conclusion NT5E-encoded CD73 may participate in the regulation of macrophage inflammatory phenotypes through adenosine signaling and may be associated with immune microenvironment remodeling at the maternal-fetal interface in RSA. Together with independent dataset validation, public single-cell exploratory analysis, and cellular experiments, these findings suggest that the adenosine-NT5E/CD73 axis may be a candidate ","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 9","pages":"798-807"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148984269","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 anti-inflammatory molecular mechanisms of shikonin].","authors":"Tong Yang, Zhenxin Ren, Tiancui Shang, Hengcai Hu, Zhiwei Wu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Shikoninis a natural naphthoquinone compound derived from plants of the Lithospermum genus, which has gained widespread attention due to its remarkable anti-inflammatory effects. In recent years, with the progressive researches on shikonin, significant advances have been made in elucidating its anti-inflammatory molecular mechanisms, laying a theoretical foundation for its application in anti-inflammatory therapy. Shikonin modulates inflammatory responses through multi-target and multi-pathway regulatory mechanisms, including suppression of pro-inflammatory cytokine expression tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), IL-1β, inhibition of classical inflammatory signaling pathways such as nuclear factor κB (NF-κB) and mitogen-activated protein kinase (MAPK) activation, and regulation of oxidative stress responses. Studies based on molecular biology, cellular experiments, and animal models have demonstrated that shikonin exhibits favorable biosafety and promising potential for drug development. However, current research still has limitations in mechanistic elucidation, pharmacokinetic data, and clinical translation. In the future, by integrating novel drug delivery systems, further exploration on the anti-inflammatory network of shikonin should be conducted to provide new strategies for the precise treatment of inflammatory diseases.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 9","pages":"851-857"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148984275","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":"[Effects and mechanisms of Jiawei Yigong San on the Th17/Treg balance in food allergy].","authors":"Xiaoxiao Lin, Zixuan Liang, Xuan Gong, Hua Liu","doi":"","DOIUrl":"","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Objective To explore the effects and mechanisms of Jiawei Yigong San (JWYGS) on the T helper type 17 (Th17)/regulatory T (Treg) cell balance in food allergy (FA). Methods Active components, action targets of JWYGS, and FA-related targets, were screened via network pharmacology. Overlapping targets between JWYGS and FA were used to construct a protein-protein interaction (PPI) network. Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) enrichment analyses were performed to predict key signaling pathways. Molecular docking was conducted to validate the binding affinity between the main active components and the predicted targets. Mice were randomly divided into control group, model group, JWYGS low-dose, medium-dose, and high-dose groups, and dexamethasone (DXM) group. An ovalbumin (OVA)-induced FA model was established. During the OVA challenge period, mice received daily intragastric administration, after which allergy and diarrhea scores were assessed. Small intestinal pathology was evaluated by HE staining. Serum ovalbumin-specific immunoglobulin E (OVA-sIgE), interleukin 6 (IL-6), IL-17, IL-2, and IL-10 were measured by ELISA. Small intestinal IL-6, IL-17, and IL-10 protein expression was detected by immunohistochemistry. Splenic Th17 and Treg cells were quantified by flow cytometry, and the Th17/Treg ratio was calculated. The mRNA expression of IL-6, retinoic acid receptor-related orphan receptor γt (RORγt), and forkhead box protein P3 (FOXP3) in the small intestine was detected by qPCR. Results Network pharmacology identified 235 active components of JWYGS and 136 common targets. GO and KEGG enrichment analyses highlighted cytokine response and Th17 differentiation. Molecular docking confirmed stable binding between core components and targets. Compared with the control group, the model group exhibited aggravated allergy and diarrhea scores, marked small intestinal inflammation and mucosal damage, elevated serum levels of OVA-sIgE, IL-6, IL-17 and IL-2, along with increased splenic Th17 cell frequency and Th17/Treg ratio. Intestinal IL-6 and IL-17 protein levels as well as IL-6 and RORγt mRNA expression were upregulated, whereas serum IL-10 levels were decreased, and intestinal expression of IL-10 protein and FOXP3 mRNA was downregulated. After JWYGS treatment, allergy and diarrhea scores were significantly reduced. Small intestinal inflammation and mucosal damage were alleviated. Serum levels of OVA-sIgE, IL-17, IL-6 and IL-2, Th17 cell frequency and the Th17/Treg ratio, intestinal IL-6 and IL-17 protein levels were decreased. IL-6 and RORγt mRNA expression was downregulated. Serum IL-10 levels were increased and intestinal expression of IL-10 protein and FOXP3 mRNA was upregulated. Moreover, the JWYGS high-dose group demonstrated comparable efficacy to the DXM group. Conclusion JWYGS can ameliorate symptoms and reverse the Th17/Treg imbalance in FA mice, potentially by inhibiting IL-6 transcription and regulating R","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 9","pages":"786-797"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148984246","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":"[Immunocyte energy metabolism imbalance and precision treatment in vitiligo: Mechanistic insights and advances in targeted intervention].","authors":"Wen Hu, Yun Qiu, Xiaojing Kang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Vitiligo is a common cutaneous depigmentation disorder with a complex pathogenesis involving multiple factors such as oxidative stress, immune response, and metabolic disorders. Recent studies have revealed that the impaired energy metabolism in immune cells is closely linked to the pathogenesis of vitiligo, with mitochondrial homeostasis disruption playing a central role. Mitochondria not only serve as the cellular energy hub but also critically regulate immune cell function and activity. Furthermore, T cells have been shown to play pivotal roles in the development of vitiligo. This review systematically summarizes the multidimensional regulatory mechanisms underlying mitochondrial dysfunction and immune cell metabolic imbalance in the onset and progression of vitiligo. It highlights recent advances in precision treatment and targeted interventions, evaluating the progress and limitations of current mitochondria-oriented strategies, including antioxidants, mitochondrial protectants, metabolic modulators, and genetic therapies. We further propose the concept of \"mitochondrial phenotype-based stratification\", emphasizing the future integration of multi-omics data and functional assessments to achieve layered precision therapy for vitiligo. This work aims to offer novel insights and a theoretical foundation for the development of new treatment strategies and drug discovery in vitiligo.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 9","pages":"818-826"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148984211","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}