International immunopharmacology最新文献

{"title":"Corrigendum to \"BOLA3 as a key protein for the treatment of diabetic skeletal muscle atrophy\" [Int. Immunopharmacol. 164 (2025) 115383].","authors":"Leiming Yang, Mi Chen, Yan Song, Qiyu Sun, Shuo Zhang, Pengyu Wang, Xiufen Liu, Qi Huang, Youzhi Zhang","doi":"10.1016/j.intimp.2025.115456","DOIUrl":"10.1016/j.intimp.2025.115456","url":null,"abstract":"","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":" ","pages":"115456"},"PeriodicalIF":4.7,"publicationDate":"2025-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to \"Didymin ameliorates hepatic injury through inhibition of MAPK and NF-κB pathways by up-regulating RKIP expression\" [Int. Immunopharmacol. 42 (2017) 130-138].","authors":"Quanfang Huang, Facheng Bai, Jinlan Nie, Shengjuan Lu, Chunyuang Lu, Xunshuai Zhu, Lang Zhuo, Xing Lin","doi":"10.1016/j.intimp.2025.115447","DOIUrl":"10.1016/j.intimp.2025.115447","url":null,"abstract":"","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":" ","pages":"115447"},"PeriodicalIF":4.7,"publicationDate":"2025-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative analysis of scRNA-seq and bulk RNA-seq to identify lactylation-related gene signatures in lung ischemia-reperfusion injury after lung transplantation.","authors":"Jiameng Gao, Xuemei Jiang, Zhiyuan Zhang, Nan Zhang, Zheyu Xia, Yu Fu, Yang Jin, Chang Chen, Zongmei Wen","doi":"10.1016/j.intimp.2025.115361","DOIUrl":"10.1016/j.intimp.2025.115361","url":null,"abstract":"<p><strong>Background: </strong>Protein lactylation has been implicated in stress-responsive cellular mechanisms, yet its role in lung transplantation-associated ischemia-reperfusion injury (IRI) remains undefined.</p><p><strong>Methods: </strong>Transcriptomic profiles from GSE145989 were analyzed through differential expression analysis (limma) and weighted gene co-expression network analysis (WGCNA). Integrating the identified genes with lactylation-related signatures uncovered key lactylation-related genes (LRGs) as potential targets. Consensus clustering stratified post-reperfusion samples into molecular subtypes with distinct lactylation dynamics. Machine learning algorithms, including least absolute shrinkage and selection operator (LASSO) and random forest, were employed to refine diagnostic biomarkers, which were subsequently incorporated into a nomogram model. External validation was performed using GSE18995 dataset, while single-cell RNA sequencing (GSE220797) was used to map cellular distributions. Lactate levels, global protein lactylation levels, and candidate gene expression were experimentally validated in a murine lung IRI model through lactic acid assay kit, western blotting, immunohistochemistry, immunofluorescence and RT-qPCR.</p><p><strong>Results: </strong>Six LRGs were identified through differential expression patterns, co-expression networks, and lactylation signatures. Consensus clustering revealed two distinct molecular subtypes with differential IRI progression patterns. Four machine learning-optimized biomarkers (SLC2A3, MYC, NLRP3, PIGA) demonstrated robust diagnostic performance. Their differential expression was confirmed in GSE18995. Single-cell data analysis revealed their predominant expression in various cell types. Murine experiments confirmed elevated lactate concentrations in bronchoalveolar lavage fluid and plasma, accompanied by enhanced global protein lactylation and consistent hub gene expression alterations.</p><p><strong>Conclusions: </strong>This integrative transcriptomic analysis identifies four lactylation-associated regulators of pulmonary IRI, proposing novel therapeutic targets for improving graft survival in lung transplantation.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":" ","pages":"115361"},"PeriodicalIF":4.7,"publicationDate":"2025-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145008282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Natsudaidain alleviates acute lung injury through the PI3K/Akt and P53 signaling pathways by inhibiting MLE-12 apoptosis: a network pharmacology study and experimental validation\" [Int. Immunopharmacol. 164 (2025) 115396].","authors":"Lijing Xia, Xiong Lei, Liwen Zhou, Xiling Liu, Pengcheng Lin, Tongtong Hou, Hanyan Xu, Shanshan Su, Li Yang, Chengshui Chen, Yuping Li","doi":"10.1016/j.intimp.2025.115464","DOIUrl":"10.1016/j.intimp.2025.115464","url":null,"abstract":"","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":" ","pages":"115464"},"PeriodicalIF":4.7,"publicationDate":"2025-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to \"Gypsophila elegans isoorientin attenuates CCl₄-induced hepatic fibrosis in rats via modulation of NF-κB and TGF-β1/Smad signaling pathways\" [Int. Immunopharmacol. 28(1) (2015) 305-312].","authors":"Xing Lin, Yongxin Chen, Shujuan Lv, Shimei Tan, Shijun Zhang, Renbin Huang, Lang Zhuo, Shuang Liang, Zhongpeng Lu, Quanfang Huang","doi":"10.1016/j.intimp.2025.115448","DOIUrl":"10.1016/j.intimp.2025.115448","url":null,"abstract":"","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":" ","pages":"115448"},"PeriodicalIF":4.7,"publicationDate":"2025-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL-36R deletion mitigates cigarette smoke-induced airway inflammation and skeletal muscle dysfunction.","authors":"Danyang Li, Jingge Qu, Yuqiang Pei, Yafei Rao, Yue Zhang, Yahong Chen, Yongchang Sun","doi":"10.1016/j.intimp.2025.115317","DOIUrl":"10.1016/j.intimp.2025.115317","url":null,"abstract":"<p><p>Chronic inflammation is a crucial driver in the development of chronic obstructive pulmonary disease (COPD) and its comorbidities, such as skeletal muscle dysfunction. Heightened IL-36 expression in the lung and systemic circulation has been observed in patients with COPD, but the potential role of IL-36 in COPD still needs further exploration. Herein, we established a COPD model through long-term cigarette smoke (CS) exposure in mice with or without IL-36R deletion. Elevated IL-36 cytokines were observed in the lung and peripheral blood of CS-exposed wild-type mice. IL-36R gene deficiency attenuated CS-induced lung parenchymal destruction and airway inflammation, as evidenced by decreased secretion of inflammatory mediators, such as IL-6, IL-1β, TNF-α and MMP9, and a diminished Th1/Tc1- and Tfh-biased immune response. In addition, skeletal muscle dysfunction was alleviated in CS-exposed mice by IL-36R deletion. Further investigations indicated that CS treatment induced the expression of IL-36 cytokines and IL-36R in C2C12 myotubes and skeletal muscles, and that IL-36 cytokines could upregulate FBXO32 and TRIM63 expression by activating NF-κB p65 pathway, thereby leading to skeletal muscle atrophy in an endocrine and autocrine/paracrine manner. Our findings provide evidence for a critical role of the IL-36/IL-36R signaling in the pathogenesis of CS-induced COPD and comorbid skeletal muscle dysfunction.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"164 ","pages":"115317"},"PeriodicalIF":4.7,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In silico analysis of VEGFR2 and c-MET in consideration with immunologic facts: Implications for mRNA vaccine design against breast cancer.","authors":"Marziyeh Ghayoumian, Fahimeh Shamsi, Hamid Madanchi, Mohammad Mehdi Ranjbar, Reza Jalalirad, Ramin Sarrami Forooshani, Mehdi Mahdavi","doi":"10.1016/j.intimp.2025.115315","DOIUrl":"10.1016/j.intimp.2025.115315","url":null,"abstract":"<p><p>Active immunization in cancer therapy can induce tumor-specific immune responses without harming the normal cells. Among these approaches, especially after the success of FDA-approved mRNA vaccines, this platform has gained much more attention as a promising strategy. This study focused on designing an mRNA-based vaccine against breast cancer by selecting two angiogenic elements that are overexpressed in breast cancer cells, in an immunoinformatic approach. Epitopes were filtered based on antigenicity, toxicity, and allergenicity to ensure that they could elicit both T and B-cell-mediated immune responses. Molecular docking simulations analyzed their interactions with Major Histocompatibility Complex (MHC) molecules. The final vaccine construct included 10 selected epitopes linked with appropriate linkers and optimized for codon usage, ensuring ideal GC content and codon adaptation index. Protein docking analyses showed strong interactions with appropriate binding energies, while molecular dynamics simulations confirmed the docked complex stability. Immune simulations revealed high antibody titers, cytokine response, and an increase in immune cells such as B Cells, Cytotoxic T Lymphocyte (CTL) cells, and Helper T Lymphocyte (HTL) cells. Based on these findings, this vaccine design presents a strong candidate for an mRNA-based breast cancer vaccine, with further development currently underway.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"164 ","pages":"115315"},"PeriodicalIF":4.7,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144816534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protein targets & therapeutics in psoriasis: toward personalization.","authors":"Mohammad Abuzar Shaikh, Ziyaul Haque, Anzarul Haque, Sanket Kumar, Mohamad Taleuzzaman","doi":"10.1016/j.intimp.2025.115331","DOIUrl":"10.1016/j.intimp.2025.115331","url":null,"abstract":"<p><p>Over 125 million individuals worldwide suffer from psoriasis, a chronic inflammatory skin condition that is immune-mediated. It is often linked to systemic comorbidities such psoriatic arthritis, cardiovascular disease, and mental health conditions. It is characterised by erythematous plaques, itching, and scaling. Psoriasis is caused by a complex interaction of environmental factors, genetic predisposition, and dysregulated immune responses, which leads to chronic inflammation and keratinocyte hyperproliferation. This review examines the treatment potential of important protein targets linked to psoriasis. Transcriptional regulators that affect inflammatory cascades and immune cell behavior include ACKR2, NFKBIZ, and TNIP1. Proteins like PK2 and KPNA2 affect the growth and differentiation of keratinocytes, and kynurenine pathway enzymes like KYNU and IDO lead to immunological imbalance. Inflammatory mediators like CXCL10 and CYR61, as well as antimicrobial peptides like LL37 and S100A15, are significantly increased in psoriatic lesions and maintain the chronic inflammatory state. Using information from the Protein Data Bank (PDB), the review also looks at the structural biology of these proteins, providing insights into molecular interactions and drug-binding sites. The study highlights the importance of these proteins in promoting individualised psoriasis treatment by combining molecular targeting techniques with new biologic treatments. This review surveys molecular proteins implicated in psoriasis, focusing on their potential as biomarkers or therapeutic targets. While many, such as CXCL10 or S100A15, are broadly involved in inflammatory cascades, others like LL37, TNIP1, and RORγt exhibit roles more uniquely tied to psoriatic pathology and may underpin future personalized treatment approaches.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"164 ","pages":"115331"},"PeriodicalIF":4.7,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144816552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging roles of KLF4 regulation of autophagy in different physiological and pathological processes.","authors":"Chenglin Zhu, Qi Zhang, Hao Fan, Xinyu Zhang, Honggang Wang","doi":"10.1016/j.intimp.2025.115350","DOIUrl":"10.1016/j.intimp.2025.115350","url":null,"abstract":"<p><p>Krüppel-like factor 4 (KLF4) is a zinc finger transcription factor that exhibits both transcriptional activation and inhibition effects. It participates in the occurrence and development of various diseases by regulating processes such as cell cycle arrest, differentiation, and the maintenance of stem cell pluripotency. Autophagy, as a conserved lysosome dependent degradation pathway in eukaryotes, maintains cellular homeostasis by clearing abnormal proteins and damaged organelles. Its dysfunction is closely related to tumors, neurodegenerative diseases, metabolic disorders, and so on. Growing evidence indicates that KLF4 participates in multiple physiological and pathological processes through regulating autophagy, however, the underlying mechanisms are not fully understood. This article systematically reviewed the understanding of KLF4 and autophagy in recent years, critically synthesized the complex and context-dependent roles of KLF4-mediated autophagy regulation in different physiological and pathological processes, and analyzed the relevant molecular mechanisms, with an emphasis on identifying overarching regulatory patterns and functional consequences, hoping to provide theoretical basis for future in-depth research.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"164 ","pages":"115350"},"PeriodicalIF":4.7,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144821332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinct STING-IRF3 activation determines IL-35⁺ Breg differentiation in rodent malaria.","authors":"Anni Feng, Qilong Li, Ning Jiang, Kunying Lv, Yixin Yang, Tong Liu, Ziwei Su, Yiwei Zhang, Xiaoyu Sang, Ying Feng, Ran Chen, Qijun Chen","doi":"10.1016/j.intimp.2025.115310","DOIUrl":"10.1016/j.intimp.2025.115310","url":null,"abstract":"<p><p>Augmented regulatory B cell (Breg) responses are commonly observed in malaria; however, the specific parasite components and Breg subtypes involved remain unclear. In this study, we investigated C57BL/6 mice infected with Plasmodium berghei ANKA, which induces cerebral malaria pathology, in comparison to P. yoelii YM, which does not. We found that distinct Breg types differentiated in response to these infections, driven by hemozoin-mediated Toll-like receptor 9 activation. Interleukin-35-positive (IL-35⁺) Breg expansion occurred in P. yoelii YM-infected mice but not in those infected with P. berghei ANKA. We demonstrated that stimulator of interferon genes (STING)-mediated interferon regulatory factor 3 (IRF3) phosphorylation suppressed IL-35⁺ Breg differentiation, potentially contributing to experimental cerebral malaria (ECM). In contrast, P. yoelii YM infection activated IRF3 in a STING-independent manner, promoting IL-35⁺ Breg expansion. These findings highlight IL-35⁺ Bregs as key modulators in malarial immunopathology.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"164 ","pages":"115310"},"PeriodicalIF":4.7,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}