Immunobiology最新文献

{"title":"Unveiling a novel NBAS mutation in common variable immunodeficiency: Expanding the genetic landscape of immunodeficiency disorders","authors":"Theresia Risa Davita ,&nbsp;Deepti Naruka ,&nbsp;Harry Lesmana ,&nbsp;James Fernandez","doi":"10.1016/j.imbio.2025.153144","DOIUrl":"10.1016/j.imbio.2025.153144","url":null,"abstract":"<div><div><em>NBAS</em>, neuroblastoma-amplified sequence, mutations have been linked to multisystem disorders, including immunodeficiency. Common variable immunodeficiency (CVID) represents a heterogeneous group of primary immunodeficiency disorders characterized by hypogammaglobulinemia, lack of functional antibodies, and frequent sinopulmonary or gastrointestinal infections. The exact cause of CVID is often unknown; however, recent studies using gene sequencing have identified disease-causing genes underlying this heterogeneous immune defect. Here, we present a case of a novel <em>NBAS</em> mutation identified in a patient with CVID, revealing the genetic basis of immunodeficiency disorders and emphasizing the importance of comprehensive genetic analysis in clinical practice. This case underscores the need for further investigation into the functional consequences of <em>NBAS</em> mutations and their implications for the management of CVID and related immune conditions.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153144"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147490895","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":"Screening of kinase-related genes as diagnostic biomarkers and immune infiltration analysis in sepsis","authors":"Bingqiang Su ,&nbsp;Yingwei Ding ,&nbsp;Xiuqi Zhu ,&nbsp;Laifa Kong","doi":"10.1016/j.imbio.2026.153158","DOIUrl":"10.1016/j.imbio.2026.153158","url":null,"abstract":"<div><h3>Background</h3><div>Sepsis is a systemic inflammatory syndrome that can lead to loss of organ function. Kinase-related genes (KRGs) modulate immune diseases by regulating inflammation, immune metabolism, and apoptosis. However, their specific role in Sepsis remains unexplored.</div></div><div><h3>Methods</h3><div>mRNA and single-cell sequencing data in sepsis were obtained from the Gene Expression Omnibus. Weighted gene co-expression network analysis (WGCNA) was used to identify gene modules associated with sepsis, which were intersected with KRGs to determine candidate genes. Functional enrichment analyses (GO, KEGG, GSVA) were conducted, followed by biomarker selection using Least Absolute Shrinkage and Selection Operator (LASSO) regression and the Boruta algorithm. Model performance was assessed via receiver operating characteristic (ROC) curves, and immune infiltration was assessed using CIBERSORT and ssGSEA. Consensus clustering defined kinase-associated molecular subtypes of sepsis, while CellChat analysis of single-cell data characterized intercellular communication patterns.</div></div><div><h3>Results</h3><div>This study employed WGCNA and machine learning analyses to identify four key diagnostic genes for sepsis—ZAP70, TXK, TRRAP, and TRIM28—and constructed a highly accurate diagnostic model (AUC = 0.986). Immune infiltration analysis revealed significant associations with T cells, NK cells, and other cell types. Single-cell data analysis demonstrated increased proportions of platelets and neutrophils in sepsis, highlighted the prominent role of monocytes in intercellular communication, and showed widespread expression of TRIM28 in monocyte subsets. Additionally, two distinct molecular subtypes with significant immune differences were identified.</div></div><div><h3>Conclusion</h3><div>This study systematically analyzed KRGs in sepsis and identified four clinically valuable biomarkers. By integrating single-cell transcriptomic data, it offers novel insights into the pathogenesis of sepsis and proposes potential biomarkers and therapeutic targets.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153158"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146029464","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":"Advances in research on the complement system and cognitive impairment","authors":"Jie Gao ,&nbsp;Zhe Li ,&nbsp;Xinyue Zhang,&nbsp;Wenshu Huang,&nbsp;Zhiyu Tian,&nbsp;Chuyu Xiao,&nbsp;Yuanyang Zhen,&nbsp;Fang Yu ,&nbsp;Xuezhao Cao","doi":"10.1016/j.imbio.2026.153157","DOIUrl":"10.1016/j.imbio.2026.153157","url":null,"abstract":"<div><div>Cognitive impairment is a global health problem with increasing prevalence and mortality rates. The complement system plays a key role in the underlying pathological mechanisms. To explore potential strategies for ameliorating and preventing cognitive impairment through targeted therapies involving the complement system, it is crucial to understand the relationship between the complement system and neuroinflammation, as well as its role in the development of cognitive dysfunction. In recent years, the mechanisms involving the complement system and its targeted treatments have become a major focus of research. This review provides an overview of the physiological functions of the complement system, its association with to neuroinflammation, the mechanisms by which it contributes to cognitive impairment, and the potential applications of complement inhibitors in the treatment of cognitive dysfunction.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 1","pages":"Article 153157"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145973287","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":"MiR-210 suppresses Candida albicans-derived β-glucan-induced inflammation in THP-1-derived macrophages via the Syk-NF-κB pathway","authors":"Junsheng Hou ,&nbsp;Min Li","doi":"10.1016/j.imbio.2026.153156","DOIUrl":"10.1016/j.imbio.2026.153156","url":null,"abstract":"<div><div>In immunocompromised individuals, infections due to <em>Candida albicans (C. albicans)</em> can be life-threatening. Recognition of the insoluble β-glucan derived from the <em>C. albicans</em> cell wall <em>(CaIG)</em> by Dectin-1 in macrophages initiates an inflammatory reaction that is critical for clearing the fungal infection. However, uncontrolled inflammation may lead to septic shock. Research has established that miR-210 is strongly upregulated in THP-1-derived macrophages (THP-1 macrophages) following <em>CaIG</em> stimulation. MiR-210 has been implicated in the metabolic and immunological responses of macrophages in various infectious and inflammatory disease models. Nevertheless, whether miR-210 modulates Dectin-1-activated inflammation remains unclear. An in vitro inflammation model was established using <em>CaIG</em>-stimulated THP-1 macrophages in the current research. By using miR-210 mimic and inhibitor transfection approaches, we observed that miR-210 overexpression significantly reduced <em>CaIG</em>-induced IL-6 and TNF-α expression, whereas inhibition of endogenous miR-210 enhanced their production. Furthermore, by inhibiting <em>CaIG</em>-triggered spleen tyrosine kinase (Syk) activation and subsequent IκBα phosphorylation, miR-210 effectively prevents the accumulation of NF-κB p65 in the nucleus in THP-1 macrophages. These findings demonstrate that miR-210 participates in negative feedback to limit <em>CaIG</em>-triggered inflammation, primarily through downregulating the Syk-NF-κB signaling cascade. In summary, our findings reveal that miR-210 acts as a precise inflammatory modulator in macrophages, highlighting its therapeutic potential.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 1","pages":"Article 153156"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145973288","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":"Single-cell transcriptome reveals that immune cells inhibit the repairment of IGFBP3 + stromal cells in thin endometrium","authors":"Haijiao Zou ,&nbsp;Dongmei Zhou ,&nbsp;Shaodan Fang ,&nbsp;Han Lin ,&nbsp;Hanzhen Xiong ,&nbsp;Qingping Jiang ,&nbsp;Mingxing Liu ,&nbsp;Xiujie Sheng ,&nbsp;Miaoxian Ou","doi":"10.1016/j.imbio.2025.153152","DOIUrl":"10.1016/j.imbio.2025.153152","url":null,"abstract":"<div><div>Thin endometrium (TE), affecting 1.5 %–9.1 % of reproductive-aged women, emerges as a disturbed decidua microenvironment underpinning implantation failure and recurrent pregnancy loss. Through integrated single-cell transcriptomics with histopathology and multiplex immunofluorescence (TSA) validation, we delineated TE as a disease of coordinated repairment impairment and pro-fibrotic remodeling across stromal and immune compartments. Key findings revealed a pathological imbalance in stromal subsets, including the decrease of regenerative IGFBP3 + Stromal_1 cells and expansion of fibrogenic Stromal_2 populations, driving collagen-dominant extracellular matrix remodeling. Concurrently, immune dysfunction was unmasked. NK cells decreased and shifted from immune surveillance to a pro-inflammatory phenotype, T cells transitioned from immune regulation to extracellular matrix remodeling effectors and macrophages adopted a pro-fibrotic phenotype with lipid metabolic collapse. CellChat analysis pinpointed suppression of GZMA-PARD3 and APOE-TREM2 axes as drivers of stromal dysfunction, while the hyperactivated adhesion (LAMA3) and collagen pathways served as central mediators of the fibro-inflammatory cascade. These findings, based on single-cell RNA-seq and spatial verification, suggest therapeutic targets for restoring endometrial homeostasis in TE. These findings suggested that TE as a disease of progressive stromal-immune fibrosis dysregulation, offering novel therapeutic targets to restore endometrial repairment and microenvironmental homeostasis.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 1","pages":"Article 153152"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145911098","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":"Predictive value of interstitial inflammation for renal outcome in patients with immunoglobulin a nephropathy","authors":"Qing Wei ,&nbsp;Min Wu ,&nbsp;Yuxiang Gong ,&nbsp;Minyu Yang ,&nbsp;Haifeng Ni ,&nbsp;Pingsheng Chen ,&nbsp;Dong Wei ,&nbsp;Xuan Shi ,&nbsp;Bin Wang ,&nbsp;Bicheng Liu","doi":"10.1016/j.imbio.2025.153150","DOIUrl":"10.1016/j.imbio.2025.153150","url":null,"abstract":"<div><h3>Background</h3><div>Renal interstitial inflammation (RII) is a common pathological feature in immunoglobulin A nephropathy (IgAN) and may predict renal outcomes, but further validation is required. This study evaluated the prognostic value of RII and inflammatory cell infiltration in patients with IgAN.</div></div><div><h3>Methods</h3><div>This retrospective cohort study included adults with biopsy-confirmed IgAN. Renal interstitial inflammation was categorised as 0 (absent), 1 (around atrophic tubules) or 2 (beyond atrophic tubules). Interstitial CD3⁺, CD20⁺ and CD68⁺ cells were quantified via immunohistochemistry. The primary outcome was a composite of a ≥ 40 % decline in the estimated glomerular filtration rate or end-stage renal disease.</div></div><div><h3>Results</h3><div>Of the 112 participating patients, 30 (26.8 %) experienced the primary outcome. A higher RII score was associated with increased risk of progression (hazard ratio for score 2 vs 0: 4.73, 95 % confidence interval [CI]: 2.01–11.13, <em>p</em> = 0.001). Patients with the outcome had higher densities of interstitial CD3⁺, CD20⁺ and CD68⁺ cells at biopsy. Kaplan–Meier analysis showed lower renal survival in patients with higher inflammatory cell densities (<em>p</em> &lt; 0.05). The RII score alone had an area under the curve of 0.804 (95 % CI: 0.715–0.894) for predicting progression, which improved to 0.865 (95 % CI: 0.779–0.951) when combined with the Oxford classification score.</div></div><div><h3>Conclusion</h3><div>The severity of RII is independently associated with renal prognosis in IgAN. Immunohistochemical evaluation of inflammatory cell infiltration may improve risk stratification and guide early intervention.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 1","pages":"Article 153150"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145911111","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":"Immunometabolism of T cells and macrophages: Human translational perspectives","authors":"Borros Arneth","doi":"10.1016/j.imbio.2025.153151","DOIUrl":"10.1016/j.imbio.2025.153151","url":null,"abstract":"<div><h3>Background</h3><div>Immunometabolism explores how immune-cell function depends on cellular energy metabolism. Recent insights demonstrate that nutrient utilization dictates activation, polarization, and tolerance.</div></div><div><h3>Aims</h3><div>To systematically review human studies on T-cell and macrophage metabolism, identify converging pathways, and outline translational implications for inflammation, autoimmunity, and cancer.</div></div><div><h3>Methods</h3><div>Following PRISMA 2020 guidelines, PubMed was searched (2015–2025) using predefined MeSH terms (“immunometabolism”, “T lymphocytes”, “macrophages”, “metabolic reprogramming”). Of 999 records, 67 met inclusion criteria (human data, peer-reviewed, quantitative endpoints). Bias was assessed with ROBIS.</div></div><div><h3>Results</h3><div>Effector T cells and M1 macrophages favor glycolysis for rapid ATP and pro-inflammatory signaling, whereas memory T cells and M2 macrophages rely on oxidative phosphorylation and fatty-acid oxidation for sustained energy and tolerance. mTORC1/AMPK signaling, glutaminolysis, and the kynurenine pathway integrate metabolic and immune cues. Metabolic dysregulation in obesity or tumor microenvironments skews these pathways, driving chronic inflammation or immune escape.</div></div><div><h3>Conclusions</h3><div>Human immunometabolism is defined by dynamic substrate switching. Targeting glycolysis, FAO, or tryptophan metabolism offers therapeutic leverage in cancer and autoimmune disease. Future directions include single-cell and spatial metabolomics and integrative metabolic-immune modeling.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 1","pages":"Article 153151"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145911149","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":"ZBP1 aggravates acute lung injury in mice by promoting the macrophage inflammatory phenotype","authors":"Hong Li ,&nbsp;Xiaoliang Du ,&nbsp;Yongze Liu,&nbsp;Jiawu Yang,&nbsp;Qinglang Dai,&nbsp;Yuan Liao,&nbsp;Feng Li","doi":"10.1016/j.imbio.2025.153154","DOIUrl":"10.1016/j.imbio.2025.153154","url":null,"abstract":"<div><h3>Background</h3><div>Acute lung injury (ALI) is an acute lung inflammatory disease that is difficult to cure and has a poor prognosis. Macrophages play a key role in the pathogenesis of ALI, and their different phenotypes and functions affect the progression of the disease. This study aimed to explore how ZBP1 affects the progression of ALI via the regulation of macrophage inflammatory phenotype.</div></div><div><h3>Methods</h3><div>A RAW264.7 cell injury model and an ALI mouse model were established via LPS induction for experimental investigation. The degree of lung injury was determined by HE staining, the protein concentration in the bronchoalveolar lavage fluid (BALF), the wet/dry weight ratio of the lung tissue, and lung myeloperoxidase (MPO) activity. The levels of related proteins, genes and inflammatory factors were detected via Western blotting, RT–qPCR and ELISA. Bioinformatics prediction and dual-luciferase reporter gene assays were used to demonstrate the interaction between miR-1298-5p and ZBP1.</div></div><div><h3>Results</h3><div>ZBP1 was highly expressed in ALI and its expression was associated with the degree of M1 macrophage polarization. ZBP1 knockdown significantly attenuated LPS-induced pathological damage to lung tissue and reduced the lung wet/dry weight ratio, protein content in BALF, MPO activity and levels of the proinflammatory cytokines IL-1β, IL-6, and TNF-α in lung tissue. Further studies revealed that ZBP1 knockdown inhibited the activation of the NF-κB signaling pathway, thereby reducing ROS levels while increasing the mitochondrial membrane potential, ATP content and expression of the mitochondrial protein TOM20, ultimately ameliorating mitochondrial dysfunction. Mechanistically, miR-1298-5p is expressed at low levels in ALI and negatively regulates ZBP1 expression. In addition, the NF-κB activator PMA reversed the inhibitory effect of ZBP1 knockdown on M1 macrophage polarization.</div></div><div><h3>Conclusion</h3><div>miR-1298-5p downregulates ZBP1 expression and inhibits NF-κB signaling pathway-mediated mitochondrial dysfunction, thereby inhibiting the M1 polarization of macrophages and the progression of ALI.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 1","pages":"Article 153154"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145911144","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":"SLAMF7 improves the efficacy of PD-1 immunotherapy by enhancing T cell response in non-small cell lung cancer","authors":"Juanfeng Lao ,&nbsp;Manman Zhu ,&nbsp;Liangjian Kuang ,&nbsp;Changliang Luo ,&nbsp;Zhongyuan Lin ,&nbsp;Qiongying Ling ,&nbsp;Yulin Yuan ,&nbsp;Yongjian Wu ,&nbsp;Liuyang Shu","doi":"10.1016/j.imbio.2026.153155","DOIUrl":"10.1016/j.imbio.2026.153155","url":null,"abstract":"<div><div>Programmed death-1 (PD-1) immune checkpoint inhibition has transformed the therapeutic landscape of non-small cell lung cancer (NSCLC), while a proportion of NSCLC cases exhibited primary or acquired resistance, reflecting the imperative to elucidate resistance mechanisms and identify synergistic immunomodulatory targets. In this context, strategies that augment the functional competence of effector T cells represent an important direction for improving immunotherapeutic efficacy. This study sought to characterize the immunological role of signaling lymphocytic activation molecule family member 7 (SLAMF7) in modulating T cell–mediated responses in non-small cell lung cancer (NSCLC). Peripheral T cells from NSCLC cases exhibited an escalated SLAMF7 expression level relative to healthy controls. Furthermore, this upregulation was more pronounced in patients who demonstrated clinical responsiveness to anti-PD-1 therapy. Moreover, SLAMF7 expression level demonstrated a positive link with both T cell abundance and the frequencies of cytokine-secreting T cell subsets. Mechanistic insights derived from a murine lung carcinoma model confirmed these outcomes. SLAMF7-deficient mice exhibited impaired anti-tumor immunity, as evidenced by accelerated tumor progression and attenuated effector cytokines production. Conversely, therapeutic co-engagement of SLAMF7 via recombinant SLAMF7 (rm-SLAMF7) plus PD-1 blockade significantly amplified anti-tumor responses, characterized by enhanced T cell expansion, activation, and cytotoxic potential. Consequently, these outcomes suggested that targeting SLAMF7 may offer a strategy to enhance PD-1-directed immunotherapy in NSCLC.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 1","pages":"Article 153155"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145973289","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":"The clinical value of combined assessment of inflammatory biomarkers and liver reserve function in predicting the 12-week prognosis of HBV-ACLF","authors":"Ke Luo,&nbsp;Tianhuang Liu","doi":"10.1016/j.imbio.2025.153147","DOIUrl":"10.1016/j.imbio.2025.153147","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) represents a serious clinical condition characterized by acute deterioration of liver function in patients with chronic liver disease. Prompt and precise prognostic assessment is key to guiding therapy and improving clinical outcomes.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Objective&lt;/h3&gt;&lt;div&gt;To investigate the clinical value of combined assessment of inflammatory biomarkers and liver reserve function indicators in predicting the 12-week prognosis of patients with HBV-ACLF.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;We analyzed clinical data from 150 HBV-ACLF patients admitted between July 2022 and December 2024. Patients were followed for 12 weeks and categorized into survival or death groups. Baseline data included inflammatory biomarkers [Neutrophil count (NEUT), Lymphocyte count (LYM), Monocyte count (MON), Platelet count (PLT), Procalcitonin (PCT)] and liver function indicators [Albumin (ALB), Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), Total bilirubin (TBIL), International normalized ratio (INR)]. Pearson correlation analysis was performed for statistically significant indicators. The construction of the combined prediction model for 12-week prognosis of HBV-ACLF was performed using multivariate logistic regression analysis. The application value of combining inflammatory biomarkers with liver reserve function indicators in the 12-week prognostic assessment of HBV-ACLF was evaluated using ROC curve analysis. &lt;em&gt;P&lt;/em&gt;-value &lt;0.05 was considered statistically significant.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Among the 150 patients with HBV-ACLF, 102 survived and 48 died. Compared to the survival group, patients in the death group were significantly older (&lt;em&gt;P&lt;/em&gt; = 0.032) and included a lower proportion of males (&lt;em&gt;P&lt;/em&gt; = 0.001). Among the laboratory indicators, the death group had significantly elevated NEUT, TBIL, INR, and PCT levels (&lt;em&gt;P&lt;/em&gt; &lt; 0.05), while LYM, PLT, and ALB levels were significantly decreased (&lt;em&gt;P&lt;/em&gt; &lt; 0.05). Pearson correlation analysis revealed that age (&lt;em&gt;r&lt;/em&gt; = 0.175, &lt;em&gt;P&lt;/em&gt; = 0.032), NEUT (&lt;em&gt;r&lt;/em&gt; = 0.184, &lt;em&gt;P&lt;/em&gt; = 0.024), TBIL (&lt;em&gt;r&lt;/em&gt; = 0.272, &lt;em&gt;P&lt;/em&gt; = 0.001), and PCT (&lt;em&gt;r&lt;/em&gt; = 0.161, &lt;em&gt;P&lt;/em&gt; = 0.049) were positively correlated with prognosis, while gender (&lt;em&gt;r&lt;/em&gt; = −0.272, &lt;em&gt;P&lt;/em&gt; = 0.001), LYM (&lt;em&gt;r&lt;/em&gt; = −0.188, &lt;em&gt;P&lt;/em&gt; = 0.021), PLT (&lt;em&gt;r&lt;/em&gt; = −0.189, &lt;em&gt;P&lt;/em&gt; = 0.021), and ALB (&lt;em&gt;r&lt;/em&gt; = −0.197, &lt;em&gt;P&lt;/em&gt; = 0.015) were negatively correlated. ROC curve analysis revealed that the AUCs for predicting the 12-week prognosis using NEUT, LYM, PLT, ALB, TBIL, and PCT alone were 0.615, 0.696, 0.616, 0.620, 0.671, and 0.608, respectively. When combined, the AUC significantly increased to 0.817 (&lt;em&gt;P&lt;/em&gt; &lt; 0.001), with a sensitivity of 79.17 % and a specificity of 76.47 %, indicating that combined indicators can more accurately predict the prognosis of","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 1","pages":"Article 153147"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145712235","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}