Immunobiology最新文献

{"title":"B lymphocytes impair osteogenesis by inhibiting BMSC differentiation in osteoporosis","authors":"Cong Peng ,&nbsp;Qiao Yang ,&nbsp;Linyu Li ,&nbsp;Yufeng Li ,&nbsp;Zhaoyang Ye ,&nbsp;Kun Zhao ,&nbsp;Yi Yi ,&nbsp;Liang Wang","doi":"10.1016/j.imbio.2025.153094","DOIUrl":"10.1016/j.imbio.2025.153094","url":null,"abstract":"<div><div><strong>Background:</strong> B lymphocytes have been implicated in the inhibition of osteogenesis, but their role in osteoporosis (OP) remains unclear. This study investigates the association between B lymphocytes and impaired osteogenesis in OP patients and explores the underlying mechanisms. <strong>Methods and materials:</strong> A retrospective analysis of 93 patients with OP assessed the relationship between B lymphocyte counts, bone formation marker Procollagen type I N-terminal propeptide (P1NP), and bone mineral density (BMD). An ovariectomy-induced OP mouse model was established. B lymphocytes and bone marrow mesenchymal stem cells (BMSCs) were isolated and co-cultured to evaluate the impact of B lymphocytes on osteogenic differentiation. Transcriptomic profiling and qPCR were performed to identify key regulatory genes. <strong>Results:</strong> Clinically, B lymphocyte counts were significantly elevated in OP patients with impaired osteogenesis (<em>P</em> &lt; 0.05). Receiver operating characteristic (ROC) analysis indicated diagnostic potential (AUC = 0.638, <em>P</em> &lt; 0.05). In vitro, B lymphocytes reduced Alkaline phosphatase (ALP) activity, calcium deposition, and the expression of osteogenic markers (<em>Osterix, Cbfa1</em>) in BMSCs. Transcriptomic analysis identified 210 differentially expressed genes, among which four (<em>Ccdc170, Extl1, Smpd3, and Thsd4</em>) were validated as potential mediators of B cell-induced osteogenesis inhibition. <strong>Conclusion:</strong> B lymphocytes may impair osteogenesis in OP by suppressing BMSC differentiation. These findings highlight B lymphocytes as potential diagnostic markers and therapeutic targets in osteoporosis.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 4","pages":"Article 153094"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144522975","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":"Untargeted metabolomics reveals postoperative metabolic dynamics in hepatic cystic echinococcosis patients","authors":"Kahaer Tuerxun ,&nbsp;Abudouxikuer Abudoumijiti ,&nbsp;Zainuer Yusupu ,&nbsp;Rousitaimujiang Yimamu ,&nbsp;Ronghua Tang ,&nbsp;Ziru Wang ,&nbsp;Abudoukeyimu Yasheng ,&nbsp;Irshat Ibrahim ,&nbsp;Yuanquan Wu","doi":"10.1016/j.imbio.2025.153099","DOIUrl":"10.1016/j.imbio.2025.153099","url":null,"abstract":"<div><h3>Background</h3><div>Hepatic cystic echinococcosis (CE) is a chronic parasitic disease caused by the larval stage of <em>Echinococcus granulosus</em> and remains a significant global zoonosis, particularly in pastoral regions of northwest China. Current diagnostic and postoperative evaluation methods, including imaging, serology, and molecular techniques, lack non-invasive, cost-effective serum biomarkers with high diagnostic accuracy.</div></div><div><h3>Objective</h3><div>This study aimed to investigate dynamic metabolic changes before and after surgery in CE patients using untargeted metabolomics analysis.</div></div><div><h3>Methods</h3><div>Serum metabolites from CE patients were analyzed using ultra-high performance liquid chromatography (UHPLC) and quadrupole time-of-flight high-resolution mass spectrometry. Samples were collected preoperatively and at 1, 4, and 12 weeks postoperatively, alongside samples from healthy controls. Four comparisons were made: preoperative patients vs. healthy controls, and postoperative samples at 1, 4, and 12 weeks vs. preoperative samples. Differential metabolites were identified using bioinformatics analysis, followed by Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment. The key metabolic pathways associated with postoperative recovery were determined by identifying shared enriched pathways across all comparisons. Metabolites in these pathways were further validated using ELISA.</div></div><div><h3>Results</h3><div>The highest number of differential metabolites was observed between preoperative CE patients and healthy controls. Postoperatively, metabolic differences increased with time. KEGG pathway enrichment revealed significant alterations in linoleic acid and arachidonic acid metabolism, both of which are linked to inflammation. ELISA confirmed elevated preoperative levels of leukotrienes, prostaglandins, thromboxanes, and inflammatory cytokines IL-5 and IL-23, which significantly declined after surgery in a time-dependent manner.</div></div><div><h3>Conclusions</h3><div>Untargeted metabolomics identified metabolites closely associated with the arachidonic acid pathway as potential biomarkers for CE diagnosis and postoperative recovery monitoring. These findings provide a foundation for developing non-invasive diagnostic and prognostic tools for hepatic cystic echinococcosis.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 4","pages":"Article 153099"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144687075","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":"LINC00461 promotes macrophage M1 polarization by inhibiting KLF4 transcription","authors":"Bicong Gao ,&nbsp;Kaitong Jia ,&nbsp;You Ya ,&nbsp;Rui Tian ,&nbsp;Xiaochen Wang ,&nbsp;Zheng Huang ,&nbsp;Feng Gao","doi":"10.1016/j.imbio.2025.153104","DOIUrl":"10.1016/j.imbio.2025.153104","url":null,"abstract":"<div><h3>Background</h3><div>Macrophage polarization is a complex process whereby macrophages differentiate into M1 (pro-inflammatory) or M2 (anti-inflammatory) phenotypes, mediating distinct and often opposing functions in immunity and tissue repair.</div></div><div><h3>Methods</h3><div>We analyzed LINC00461 expression in M1- and M2-polarized macrophages using qPCR. Functional assays (<em>in vitro</em> and <em>in vivo</em>) were performed to assess the effects of LINC00461 knockdown on cytokine secretion. RNA-seq, bisulfite sequencing, and chromatin immunoprecipitation (ChIP) were used to explore the mechanism involving Kruppel-like factor 4 (KLF4) and DNA methylation.</div></div><div><h3>Results</h3><div>LINC00461 levels were elevated in M1 macrophages and reduced in M2 macrophages. Knockdown of LINC00461 attenuated pro-inflammatory cytokine release (e.g., IL-1β, TNF-α) in M1 cells and promoted anti-inflammatory cytokine secretion (e.g., IL-10, TGF-β) in M2 cells. Mechanistically, LINC00461 knockdown upregulated <em>KLF4</em> transcription, a key M2 polarization regulator. LINC00461 recruited DNA methyltransferases to induce hypermethylation of the <em>KLF4</em> promoter, suppressing KLF4 expression and driving M1 polarization.</div></div><div><h3>Conclusion</h3><div>Our findings establish a functional link between LINC00461, <em>KLF4</em> methylation, and macrophage polarization, providing insights into the epigenetic regulation of inflammatory responses.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 4","pages":"Article 153104"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144694563","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":"Amyloid β (Aβ) inhibits retinal angiogenesis in Alzheimer's disease via LncRNA-XIST/miRNA-126-5p/VEGF axis","authors":"Bin Wang ,&nbsp;Wenwei Li ,&nbsp;Chaoyang Hong ,&nbsp;Fangfang Jin ,&nbsp;Baisheng Xu ,&nbsp;Zhongwei Guo ,&nbsp;Shuyang Chen ,&nbsp;Qi Zhang","doi":"10.1016/j.imbio.2025.153097","DOIUrl":"10.1016/j.imbio.2025.153097","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is often accompanied by retinal lesions, in which Amyloid β (Aβ) is a key mediator. Vascular dysfunction is always associated with the malignant progression of AD, but the precise mechanisms remain poorly understood. The aim of this study is to investigate how Aβ regulates retinal angiogenesis in AD models through the LncRNA-XIST/miR-126-5p/VEGF axis. The research results showed that in the retina of AD model mice, the expression of Aβ and miR-126-5p increased, while the expression of LncRNA-XIST and VEGF decreased. In vitro experiments demonstrated that Aβ treatment downregulated LncRNA-XIST and VEGF expression in RF/6 A cells, while upregulating miR-126-5p and significantly suppressing angiogenesis. Overexpression of LncRNA-XIST can reverse the inhibitory effect of Aβ on angiogenesis, while further overexpression of miR-126-5p can counteract the pro-angiogenic effect of LncRNA-XIST. The dual-luciferase reporter assay results showed that Aβ repressed the transcriptional activity of the LncRNA-XIST promoter by targeting the −800 to −600 fragment. Mechanism studies have revealed that LncRNA-XIST competitively binds to miR-126-5p, preventing its binding to VEGF mRNA and upregulating VEGF expression. In vivo experiments demonstrated that miR-126-5p inhibitor resulted in elevated expression of LncRNA-XIST and VEGF in the mouse retina. This study reveals the molecular mechanism by which Aβ regulates retinal angiogenesis in AD models through the LncRNA-XIST/miR-126-5p/VEGF axis, providing a potential new strategy for targeted therapy of AD-related retinal lesions.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 4","pages":"Article 153097"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144656500","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":"Serum LINC01278 serves as a negative biomarker for sepsis and its up-regulation inhibits LPS-induced inflammatory response in THP-1 cells","authors":"Ying Gu,&nbsp;Honggang Jia,&nbsp;Xinyu Lin,&nbsp;Ling Wang","doi":"10.1016/j.imbio.2025.153098","DOIUrl":"10.1016/j.imbio.2025.153098","url":null,"abstract":"<div><h3>Background</h3><div>Sepsis represents a potentially fatal condition characterized by organ failure. Long non-coding RNAs (lncRNAs) have provided new insights into the treatment of inflammation caused by sepsis.</div></div><div><h3>Aims</h3><div>Exploring the involvement of <em>LINC01278</em> in sepsis and lipopolysaccharide (LPS)-induced inflammatory responses.</div></div><div><h3>Methods</h3><div>A sepsis cell model was established by stimulating THP-1 cells with LPS. Cell proliferation was assessed with the CCK-8 assay, while apoptotic cells were quantified through flow cytometric analysis. The expression of <em>LINC01278</em> and miR-451a, along with the interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β), were measured using RT-qPCR and ELISA, respectively. Bioinformatics tools were used to predict the targeting relationship between <em>LINC01278</em> and miR-451a, and their direct interaction was validated by Dual-luciferase reporter assays and RNA immunoprecipitation (RIP).</div></div><div><h3>Results</h3><div>Serum <em>LINC01278</em> expression was significantly lower in 108 sepsis patients than in 105 healthy controls. ROC curve and Kaplan-Meier results indicated that <em>LINC01278</em> had a good diagnostic efficacy for sepsis and was negatively associated with poor prognosis. <em>LINC01278</em> overexpression promoted cell viability, inhibited apoptosis, and reduced the production of IL-6, TNF-α, and IL-1β. Bioinformatics analysis identified miR-451a, which was upregulated in septic patients, as a potential target of <em>LINC01278</em>. Dual-luciferase reporter assays, along with RIP experiments, have verified that <em>LINC01278</em> functions as a competitive endogenous RNA (ceRNA) for miR-451a.</div></div><div><h3>Conclusions</h3><div><em>LINC01278</em> serves as a clinical indicator for both diagnosing sepsis and assessing disease severity. <em>LINC01278</em> exerts protective effects in sepsis by acting as a ceRNA for miR-451a.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 4","pages":"Article 153098"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144702673","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":"Liyan Kaiyin Formula relieves reflux pharyngitis by regulating M1 macrophage polarization via the NF-κB/NLRP3 pathway","authors":"Lirong Wang ,&nbsp;Xuqing Chen ,&nbsp;Tianyu Xu ,&nbsp;Youpeng Fei ,&nbsp;Qi Yang ,&nbsp;Jingjuan An ,&nbsp;Zeqing Li ,&nbsp;Kunmin Wu","doi":"10.1016/j.imbio.2025.153095","DOIUrl":"10.1016/j.imbio.2025.153095","url":null,"abstract":"<div><div><em>Background:</em> We aimed to investigate whether Liyan Kaiyin Formula (LYKYF) can relieve reflux pharyngitis in rats by regulating M1 macrophage polarization <em>via</em> the nuclear factor-κB (NF-κB)/Nod-like receptor protein 3 (NLRP3) pathway.</div><div><em>Methods:</em> Forty rats were randomized into a sham group, a laryngopharyngeal reflux disease (LPRD) group, a LYKYF group and a LYKYF+CHPG group (<em>n</em> = 10). Enzyme-linked immunosorbent assay was conducted to measure the serum levels of inflammatory factors interleukin-6 (IL-6), IL-1β and tumor necrosis factor-α (TNF-α). Western blotting and reverse transcription-polymerase chain reaction (RT-PCR) were performed to measure the expressions of proteins implicated in NF-κB/NLRP3 pathway. Western blotting was also used for the detection of M1 macrophage markers (CD86 and iNOS).</div><div><em>Results:</em> Compared to the sham group, TNF-α, IL-6 and IL-1β levels in the serum, proportion of M1 macrophages in pharyngeal tissues, p-NF-κB p65/p65 ratio, protein expressions of NLRP3, Caspase-1, Apoptosis-associated speck-like protein (ASC), cluster of differentiation 86 (CD86) and inducible nitric oxide synthase, and mRNA expressions of NF-κB p65, NLRP3, Caspase-1 and ASC in the LPRD group exhibited significant elevations (<em>P</em> &lt; 0.05). Compared with the LYKYF group, the LYKYF+CHPG group had significant elevations in serum TNF-α, IL-6 and IL-1β levels, proportion of M1 macrophages in pharyngeal tissues, p-NF-κB p65/p65 ratio, protein expressions of NLRP3, Caspase-1, ASC, CD86 and iNOS, as well as NF-κB p65, NLRP3, Caspase-1 and ASC mRNA expressions (<em>P</em> &lt; 0.05). The identified key target genes were significantly enriched in GO terms associated with signal transduction, protein phosphorylation regulation, and adaptive responses to external stimuli.</div><div><em>Conclusion:</em> LYKYF may suppress M1 macrophage polarization through suppressing the NF-κB/NLRP3 pathway activation, thereby alleviating reflux pharyngitis in rats.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 4","pages":"Article 153095"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144518308","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":"Exosomes derived from baicalin-pretreated bone marrow mesenchymal stem cells inactivate the TLR4/MyD88/NF-kB pathway to improve asthma","authors":"Wenbo Shen ,&nbsp;Wei Jia ,&nbsp;Qiang Wu ,&nbsp;Li Shen ,&nbsp;Yisheng Wang","doi":"10.1016/j.imbio.2025.153103","DOIUrl":"10.1016/j.imbio.2025.153103","url":null,"abstract":"<div><h3>Background</h3><div>Baicalin, a natural compound isolated from the root of <em>Scutellaria baicalensis Georgi</em>, has been shown to have various pharmacological effects on lung diseases including asthma. Recently, research has suggested that baicalin combined with exosomes may have significant potential against disease development. The present work analyzes the effects of exosomes derived from baicalin-pretreated bone marrow mesenchymal stem cells (BMSCs) on asthma and the underlying mechanism.</div></div><div><h3>Methods</h3><div>BALB/c mice were sensitized with ovalbumin (OVA) through intraperitoneal injection to establish an animal model of asthma. Human bronchial epithelial cells (16HBE) were exposed to lipopolysaccharide to mimic a cell model of asthma. The pathological conditions of lung tissues in OVA-induced mice were analyzed by haematoxylin and eosin staining assays. Masson staining and quantification analysis were conducted to analyze percentage of collagen fibers in lung tissues of OVA-induced mice. The Wright-Giemsa assay was used to determine the number of eosinophils, neutrophils, lymphocytes and macrophages. Enzyme-linked immunosorbent assays were performed to analyze expression levels of inflammatory factors including IL-4, IL-5, IL-13 and TNF-α levels. The values of airway resistance (Rrs), elastance (Ers) and compliance (Crs) were recorded for analyzing airway hyperresponsiveness through the FlexiVent system. Protein expression was analyzed by immunohistochemistry (IHC) and/or western blotting assay.</div></div><div><h3>Results</h3><div>Ovalbumin (OVA) pretreatment increased airway inflammation, airway hyperresponsiveness, collagen deposition and epithelial-mesenchymal transition (EMT) in mice, however, these phenomena were significantly improved after treatment with baicalin-pretreated BMSC exosomes. Lipopolysaccharide (LPS)-induced 16HBE cells showed increased levels of interleukin-4 (IL-4), interleukin-5 (IL-5), interleukin-13 (IL-13) and tumor necrosis factor-α (TNF-α), elevated N-cadherin and Vimentin protein expression, and decreased E-cadherin protein expression, whereas these LPS-induced effects were relieved after treatment with baicalin-pretreated BMSC exosomes. Additionally, protein expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response protein 88 (MyD88) and phosphor p65 (p-p65) was upregulated in lung tissues of OVA-induced mice and LPS-stimulated 16HBE cells, but these phenomena were counteracted following exosomes treatment from baicalin-pretreated BMSCs.</div></div><div><h3>Conclusion</h3><div>Exosomes derived from baicalin-pretreated BMSCs ameliorated airway inflammation, airway hyperresponsiveness and airway remodeling after asthma by inactivating the TLR4/MyD88/nuclear factor kappa B pathway, providing a therapeutic strategy for asthma.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 4","pages":"Article 153103"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144670606","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":"Diversity and hallmarks of metabolites surveyed by MR1","authors":"Emi Ito ,&nbsp;Sho Yamasaki","doi":"10.1016/j.imbio.2025.153091","DOIUrl":"10.1016/j.imbio.2025.153091","url":null,"abstract":"<div><div>Mucosal-associated invariant T (MAIT) cells are one of the innate T cell subset. They are known to contribute to anti-bacterial response by recognizing bacterial components with invariant TCRs which are presented on a monomorphic antigen presenting molecule, MHC related protein 1(MR1). After years of uncertainty about the molecular entity of this bacterial antigen, they were recognized as vitamin B metabolites in 2012, and identified as 5-OP-RU in 2014. Recently, MR1 was found to contain a broad ligand-binding pocket, allowing recognition of compounds with various structures. In this review article, we will summarize the history of MR1 ligand discovery and discuss the potential new ligand structures that may uncover previously-unappreciated MAIT cell functions.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 4","pages":"Article 153091"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144597588","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":"Low peripheral blood B lymphocyte count predicts poor outcome in patients with multiple myeloma","authors":"Yuqi Wang ,&nbsp;Zhongxin Zheng ,&nbsp;Qiaoxi Kang ,&nbsp;Linjing Cai ,&nbsp;Shanshan Zhang ,&nbsp;Huan Chen ,&nbsp;Youhai Yuan ,&nbsp;Hanzhen Zhang ,&nbsp;Xiaolei Wei ,&nbsp;Ru Feng ,&nbsp;Yongqiang Wei","doi":"10.1016/j.imbio.2025.153096","DOIUrl":"10.1016/j.imbio.2025.153096","url":null,"abstract":"<div><div>Previous evidence suggested that B lymphocytes may be involved in the progression and prognosis of multiple myeloma (MM). However, the prognostic value of peripheral B lymphocyte counts on MM before and after treatment in the novel agent era was rarely reported. Herein, we conducted a retrospective study in our center to detect peripheral B lymphocyte counts by flow cytometry in 110 patients with MM and explore the relation with survival. The B lymphocyte count was significantly lower in MM patients than healthy controls (<em>p</em> &lt; 0.005). The cutoff value of B lymphocyte count at diagnosis was 49/μl in MM and 94 patients were divided into in high B lymphocyte group. Patients with low B lymphocyte count had a significant shorter progression-free survival (PFS) (<em>p</em> = 0.025) and a trend of unfavorable overall survival (OS) (<em>p</em> = 0.053) at diagnosis and after 4 cycles' induction treatments. Furthermore, Multivariate analysis showed that low B lymphocyte count at diagnosis independent of ISS stage was a significantly inferior marker for predicting PFS (<em>p</em> = 0.027, hazard ratio(HR) 2.281, 95 % confidence interval (CI) 1.098–4.741) and a trend for OS (<em>p</em> = 0.083, HR 2.394, 95 % CI 0.896–6.160). In summary, these results suggested the low B lymphocyte count was associated with poor outcome in MM patients at diagnosis and after treatment in the novel agent era.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 4","pages":"Article 153096"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144579294","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":"Quantification and clustering of immune states in hepatitis B Cirrhosis","authors":"Wei Hou ,&nbsp;Tengxiao Liang ,&nbsp;Fangliang Xing ,&nbsp;Zhongjie Hu","doi":"10.1016/j.imbio.2025.153093","DOIUrl":"10.1016/j.imbio.2025.153093","url":null,"abstract":"<div><h3>Background</h3><div>Hepatitis B Cirrhosis, a severe progression of chronic Hepatitis B infection, requires a comprehensive understanding of the interplay among lymphocyte populations. This study aims to quantify and visualize the relationships among T cells, NK cells, and B cells to aid in assessing immune status, diagnosing the condition, and optimizing treatment strategies.</div></div><div><h3>Methods</h3><div>Peripheral blood samples were collected from 500 patients diagnosed with Hepatitis B Cirrhosis and 500 healthy controls. Sort visualization analysis and three-dimensional numerical fitting were performed to establish a mathematical model describing the relationships among lymphocyte subsets. Self-Organizing Feature Maps (SOFM) were employed for unsupervised clustering to identify distinct immune states.</div></div><div><h3>Results</h3><div>Sort visualization analysis revealed a gradual decrease in T + NK cell levels as B cell levels increased, demonstrating a clear inverse relationship. SOFM clustering identified three distinct clusters with well-defined boundaries. In the 3D lymphocyte plane described by the eq. T percentage =  ‐−0.9879 × B percentage - 1.041 × NK percentage + 97.66, a significant contrast was observed between Hepatitis B Cirrhosis samples and the healthy sample baseline. Analysis across Child-Pugh grades uncovered a cyclical pattern in immune states, reflecting the various stages of the viral infection process.</div></div><div><h3>Conclusions</h3><div>This study provides a quantitative mathematical model and visual representation of lymphocyte population dynamics in Hepatitis B Cirrhosis. The identification of distinct immune states associated with disease progression facilitates the assessment of immunological condition and the optimization of treatment strategies. The integration of immunological and clinical data opens new possibilities for more precise disease staging and personalized.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 4","pages":"Article 153093"},"PeriodicalIF":2.5,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144510819","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}