International immunopharmacology最新文献

{"title":"Effects of immune response on different nano-adjuvants combined with H11 antigen of Haemonchus contortus","authors":"Lisha Ye,&nbsp;Tianjiao Wang,&nbsp;Simin Wu,&nbsp;Hui Liu,&nbsp;Feng Liu,&nbsp;Chunqun Wang,&nbsp;Min Hu","doi":"10.1016/j.intimp.2024.113602","DOIUrl":"10.1016/j.intimp.2024.113602","url":null,"abstract":"<div><div>The intestinal native protein H11 is one of the most immunodominant antigen of <em>Haemonchus contortus</em>. However, H11 combined with QuilA adjuvant shows only short-lived protection for animals. Nano-adjuvants have the huge potential to extend the immune response in human and animals. Here, we compared the immune responses induced by H11 combined with three nano-adjuvants including lipid nanoparticles (LNP), immunostimulating complex matrix (IMX) and AddaS03™. We measured the cytokine levels of goat PBMCs stimulated by H11 mixed with three nano-adjuvants and QuilA. Results showed that the transcriptions of IL-6, IL-8 and IFN-γ genes were significantly inhibited in all adjuvant group compared with PBS control. H11-IMX combination significantly up-regulated IL-2, IL-17 and TNF-α gene transcriptions. The H11-LNP group showed a significant increase in IL-17 and TNF-α transcriptions, while the H11-AddaS03™ group significantly increased IL-2 transcription. Additionally, mice immunized with these formulations were assessed for splenic lymphocyte proliferation. All H11-adjuvant combinations, except H11-LNP, significantly stimulated lymphocyte proliferation compared to the H11 alone and PBS control groups, with the H11-AddaS03™ combination showing the strongest effect. Analysis of serum antibody levels revealed that all immune groups induced high IgM levels, with H11-IMX inducing the highest IgG levels. Our results demonstrated that IMX or LNP combined with H11 mainly induced a Th17 cell immune response in goat PBMCs, while IMX or AddaS03™ combined with H11 could induce a strong humoral immune response in mice. This study elucidates the immune response profiles of different nano-adjuvant combined with H11 antigen, providing important insights for vaccine development against parasitic nematodes.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"143 ","pages":"Article 113602"},"PeriodicalIF":4.8,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619513","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":"Notoginsenoside R1-Protocatechuic aldehyde reduces vascular inflammation and calcification through increasing the release of nitric oxide to inhibit TGFβR1-YAP/TAZ pathway in vascular smooth muscle cells","authors":"Xinhai Cui ,&nbsp;Lei Zhang ,&nbsp;Lin Lin ,&nbsp;Yuanlong Hu ,&nbsp;Muxin Zhang ,&nbsp;Bowen Sun ,&nbsp;Zhiyuan Zhang ,&nbsp;Mengkai Lu ,&nbsp;Xiuya Guan ,&nbsp;Jiaqi Hao ,&nbsp;Yunlun Li ,&nbsp;Chao Li","doi":"10.1016/j.intimp.2024.113574","DOIUrl":"10.1016/j.intimp.2024.113574","url":null,"abstract":"<div><div>Vascular calcification is a significant factor contributing to the rupture of vulnerable atherosclerotic plaques, ultimately leading to cardiovascular disease. However, no effective treatments are currently available to slow the progression of vascular calcification. Notoginsenoside R1 (R1) and protocatechuic aldehyde (PCAD), primary active components extracted from <em>Panax notoginseng</em> and <em>Salvia miltiorrhiza</em> Burge, have shown potential in mitigating endothelial injury and atherosclerosis. This study investigated the effects of R1-PCAD on nitric oxide (NO) production in endothelial cells (ECs) and its role in counteracting vascular calcification and inflammation. Additionally, it explored the mechanisms underlying these effects. To simulate atherosclerotic calcification, apolipoprotein E-deficient (ApoE^−/−) mice were fed a high-fat diet and given intraperitoneal injections of vitamin D3. Treatment with the R1-PCAD combination improved endothelial function, reduced inflammation in the aorta, and lowered calcium deposition. Mechanistically, R1-PCAD enhanced eNOS-Ser1177 phosphorylation by activating the AMPKα/Akt pathway, which stimulated NO production and eNOS activation in ECs. In an <em>in vitro</em> co-culture model involving vascular smooth muscle cells (VSMCs) and ECs, R1-PCAD similarly reduced inflammation and calcification in VSMCs triggered by β-glycerophosphate, with these effects partially dependent on NO levels and EC functionality. Further investigation revealed that R1-PCAD facilitated NO release from ECs, which subsequently inhibited TGFβR1 activation in VSMCs. This inhibition reduced Smad2/3 activation and nuclear translocation of YAP/TAZ, thereby diminishing inflammation and calcification in VSMCs. These findings suggest that R1-PCAD alleviates vascular inflammation and calcification primarily via the NO-TGFβR1-YAP/TAZ signaling pathway. This study presents a promising new approach for treating vascular calcification by targeting intercellular signaling pathways.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"143 ","pages":"Article 113574"},"PeriodicalIF":4.8,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619450","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":"Insight of immune checkpoint inhibitor related myocarditis","authors":"Jin-kui Pi ,&nbsp;Xiao-ting Chen ,&nbsp;Yan-jing Zhang ,&nbsp;Xue-mei Chen ,&nbsp;Yin-chan Wang ,&nbsp;Jia-yi Xu ,&nbsp;Jin-han Zhou ,&nbsp;Shuai-shuai Yu ,&nbsp;Si-si Wu","doi":"10.1016/j.intimp.2024.113559","DOIUrl":"10.1016/j.intimp.2024.113559","url":null,"abstract":"<div><div>As the understanding of immune-related mechanisms in the development and progression of cancer advances, immunotherapies, notably Immune Checkpoint Inhibitors (ICIs), have become integral in comprehensive cancer treatment strategies. ICIs reactivate T-cell cytotoxicity against tumors by blocking immune suppressive signals on T cells, such as Programmed Death-1 (PD-1) and Cytotoxic T-lymphocyte Antigen-4 (CTLA-4). Despite their beneficial effects, ICIs are associated with immune-related adverse events (irAEs), manifesting as autoimmune side effects across various organ systems. A particularly alarming irAE is life-threatening myocarditis. This rare but severe side effect of ICIs leads to significant long-term cardiac complications, including arrhythmias and heart failure, and has been observed to have a mortality rate of up to 50% in affected patients. This greatly limits the clinical application of ICI-based immunotherapy. In this review, we provide a comprehensive summary of the current knowledge regarding the diagnosis and management of ICI-related myocarditis. We also discuss the utility of preclinical mouse models in understanding and addressing this critical challenge.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"143 ","pages":"Article 113559"},"PeriodicalIF":4.8,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619521","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":"4-Hydroxyphenylacetic Acid, a microbial-derived metabolite of Polyphenols, inhibits osteoclastogenesis by inhibiting ROS production","authors":"Zhanchi Zhang ,&nbsp;Junchuan Liu ,&nbsp;Yijun Li ,&nbsp;Yunsheng Wang ,&nbsp;Xiao Zheng ,&nbsp;Feng Wang ,&nbsp;Tong Tong ,&nbsp;Dechao Miao ,&nbsp;Wenshuai Li ,&nbsp;Lei Chen ,&nbsp;Linfeng Wang","doi":"10.1016/j.intimp.2024.113571","DOIUrl":"10.1016/j.intimp.2024.113571","url":null,"abstract":"<div><div>Intracellular reactive oxygen species (ROS) accumulation is key to osteoclast differentiation. Plant-derived polyphenols that have reduced ROS production have been widely studied for the treatment of osteoporosis. However, these compounds are rarely absorbed in the small intestine and are instead converted to phenolic acids by the microbiota in the colon. These large quantities of low-molecular-weight phenolic acids can then be absorbed by the body. 4-Hydroxyphenylacetic acid (4-HPA) is an important metabolite of these polyphenols that is generated by the human intestinal microbiota. However, its potential mechanism is not fully understood.</div><div>In this study, we aimed to elucidate the role of 4-HPA on osteoclastogenesis and treating osteoporosis. Our study showed that 4-HPA inhibited osteoclast differentiation and function and downregulated osteoclast-specific genes, including <em>NFATc1</em>, <em>Atp6v0d2</em>, <em>MMP9</em>, <em>CTSK</em>, <em>Acp5</em>, and <em>c-Fos</em>. As for further mechanism exploration, 4-HPA reduced ROS accumulation by regulating nuclear factor erythroid 2-related factor (Nrf2) and subsequently inhibited the nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways. To evaluate the effect of 4-HPA on postmenopausal osteoporosis, an ovariectomized (OVX) mouse model was used. The Micro-CT and histomorphometry analyses showed that 4-HPA effectively prevents bone loss. Encouragingly, 4-HPA demonstrated efficacy in treating osteoporosis induced by OVX.</div><div>In conclusion, our study revealed that 4-HPA, a polyphenol metabolite produced by intestinal microorganisms, also inhibits osteoclast formation and treats osteoporosis, which provides a new experimental basis and candidate drug for the treatment of osteoporosis.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"143 ","pages":"Article 113571"},"PeriodicalIF":4.8,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619478","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":"OSU-T315 overcomes immunosuppression in triple-negative breast cancer by targeting the ILK/NF-κB signaling pathway to enhance immunotherapeutic efficacy","authors":"Yi Wang ,&nbsp;Yuenong Qin ,&nbsp;Chunyu Wu ,&nbsp;Jiajing Chen ,&nbsp;Yang Zhang ,&nbsp;Yueqiang Chen ,&nbsp;Xiaohong Xie ,&nbsp;Xiufei Gao ,&nbsp;Chenping Sun ,&nbsp;Sheng Liu","doi":"10.1016/j.intimp.2024.113530","DOIUrl":"10.1016/j.intimp.2024.113530","url":null,"abstract":"<div><div>Triple negative breast cancer (TNBC) is an aggressive and immunogenic subtype of breast cancer. The absence of biomarker has given immune checkpoint inhibitors (ICIs) a broad prospect in this type of breast cancer. The infiltration of regulatory T cells (Tregs) expressing transcription factor forkhead box P3 (Foxp3) in the tumor microenvironment (TME) is the key factor leading to ICIs resistance. Therefore, elimination of tumor antigen-specific Tregs may be an important aspect of improving ICIs efficacy. In this study, it based on the Gene Expression Omnibus and The Cancer Genome Atlas database, along with in vivo and in vitro experimental models, to verified that the high expression of integrin-linked kinase (<em>ILK</em>) in TNBC is the key differential factor leading to the high infiltration of Foxp3⁺-Tregs in the TME. Then, we selected ILK-specific inhibitor, OSU-T315, to intervene in vitro and vivo. Importantly, we found that OSU-T315 blocked the secretion of CCL17/CCL22 in tumor cells by inhibiting the ILK/NF-κB pathway, resulting in the apoptosis of Foxp3⁺-Tregs and decreased programmed cell death-1 (PD-1) expression. Therefore, our findings indicate a novel mechanism of OSU-T315 with potential therapeutic application in TNBC.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"143 ","pages":"Article 113530"},"PeriodicalIF":4.8,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PNSC5325 prevents acute respiratory distress syndrome by alleviating inflammation and inhibiting extracellular matrix degradation of alveolar macrophages","authors":"Fan Li ,&nbsp;Wenqing Yan ,&nbsp;Zhiping Chen ,&nbsp;Weihua Dong ,&nbsp;Zhi Chen","doi":"10.1016/j.intimp.2024.113579","DOIUrl":"10.1016/j.intimp.2024.113579","url":null,"abstract":"<div><h3>Background</h3><div>Acute respiratory distress syndrome (ARDS) is characterized by severe inflammation and significant extracellular matrix (ECM) degradation in the lungs. Our prior research identified the CtBP2-p300-NF-κB (C-terminal-binding protein 2-histone acetyltransferase p300-nuclear factor kappa B) transcriptional complex as critical in ARDS by activating pro-inflammatory cytokine genes.</div></div><div><h3>Methods</h3><div>An ARDS mouse model was established using intratracheal instillation of lipopolysaccharide (LPS). Small molecules that inhibit the CtBP2-p300 interaction were identified through AlphaScreen. RNA sequencing (RNA-Seq) was conducted to determine differential gene expression. Immunoprecipitation and co-immunoprecipitation analyzed protein interactions. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and immunoblotting detected gene and protein expression. Histological staining evaluated tissue damage.</div></div><div><h3>Results</h3><div>Through AlphaScreen, two natural compounds, PNSC2477 and PNSC5325, were identified for their ability to inhibit the CtBP2-p300 interaction. While PNSC2477 demonstrated toxicity and was deemed unsuitable for further research, PNSC5325 exhibited minimal toxicity. PNSC5325 effectively inhibited the CtBP2-p300 interaction and reduced pro-inflammatory cytokine gene expression. RNA-Seq analysis of PNSC5325-treated cells indicated significant suppression of pro-inflammatory cytokine genes and matrix metalloproteinases (<em>MMPs</em>). Further molecular studies revealed that the CtBP2-p300 complex, in conjunction with activator protein 1 (AP1), activates <em>MMP</em> expression. PNSC5325 simultaneously suppressed both pro-inflammatory cytokines and <em>MMPs</em> by targeting the CtBP2-p300 complex. In LPS-injected mice, PNSC5325 administration significantly reduced ARDS incidence by inhibiting inflammatory and <em>MMP</em> genes.</div></div><div><h3>Conclusion</h3><div>These findings suggest that PNSC5325 protects against ARDS by inhibiting key inflammatory and ECM degradation pathways, highlighting its potential as a novel therapeutic agent for ARDS and paving the way for further clinical investigations.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"143 ","pages":"Article 113579"},"PeriodicalIF":4.8,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619581","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":"Polymethoxylated flavones for modulating signaling pathways in inflammation","authors":"Lixia Yue ,&nbsp;Ning Li ,&nbsp;Xianglu Ye ,&nbsp;Yanfeng Xiu ,&nbsp;Bing Wang","doi":"10.1016/j.intimp.2024.113522","DOIUrl":"10.1016/j.intimp.2024.113522","url":null,"abstract":"<div><div>Aberrant signaling pathways play a crucial role in the pathogenesis of various diseases, including inflammatory disorders and autoimmune conditions. Polymethoxylated flavones (PMFs), a class of natural compounds found in citrus fruits, have obtained increasing attention for their potential therapeutic effects in modulating inflammatory responses. Although significant progress has been made in the pharmacological research of PMFs, the mechanisms by which they modulate signaling pathways to treat inflammation have not been systematically reviewed or analyzed. To address this gap in the literature, this review explores the mechanisms underlying the anti-inflammatory properties of PMFs and their prospects as drugs for treating inflammatory diseases. We discuss the molecular targets and signaling pathways through which PMFs exert their anti-inflammatory effects, including NF-κB pathway, PI3K/Akt pathway, MAPK pathway, Nrf2 pathway, and regulation of inflammatory cytokine production. Furthermore, we highlight preclinical studies evaluating the efficacy of PMFs in various inflammatory conditions, such as rheumatoid arthritis (RA), inflammatory bowel disease (IBD), and osteoarthritis (OA). Despite promising findings, challenges remain in optimizing the pharmacokinetic properties and therapeutic efficacy of PMFs for clinical use. Future research directions include elucidating the structure–activity relationships of PMFs, developing novel delivery strategies, and conducting large-scale clinical trials to validate their efficacy and safety profiles. Overall, PMFs represent a promising class of natural compounds with potential applications as anti-inflammatory drugs, offering novel therapeutic opportunities for managing inflammatory diseases.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"143 ","pages":"Article 113522"},"PeriodicalIF":4.8,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604007","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":"Molecular characterization of PANoptosis-related genes associated with immune infiltration and prognosis in idiopathic pulmonary fibrosis","authors":"Hongzuo Chen,&nbsp;Zhenkun Xia,&nbsp;Bei Qing,&nbsp;Linguo Gu,&nbsp;Ying Chen,&nbsp;Juan Wang,&nbsp;Yunchang Yuan","doi":"10.1016/j.intimp.2024.113572","DOIUrl":"10.1016/j.intimp.2024.113572","url":null,"abstract":"<div><div>Idiopathic pulmonary fibrosis (IPF) is a chronic pulmonary disease with unknown pathogenesis and poor prognosis. PANoptosis, a newly identified form of inflammatory programmed cell death, has been implicated in various inflammatory lung diseases. This study aimed to identify differentially expressed PANoptosis-related genes (PRDEGs) associated with immune infiltration and prognosis in IPF, while also establishing a novel prognostic prediction model. A total of 63 PRDEGs were identified from GSE110147 dataset, with 31 exhibiting consistent expression trends in GSE213001. Enrichment analysis indicated that the majority of these PRDEGs were enriched in inflammatory and immune-related pathways. Three key PRDEGs—NLRP3, ATM, and VEGFA—were selected through univariate and multivariable Cox regression analyses. The prognostic prediction model developed from these key PRDEGs demonstrated robust predictive performance. Furthermore, the expression of most PRDEGs was positively correlated with pro-inflammatory immune cells, including macrophages, neutrophils, and CD4⁺ T cells. Validation of the expression levels of these key PRDEGs was conducted in fibrotic mouse lung tissue. This study suggests that PANoptosis plays a role in IPF, potentially linked to the infiltration of pro-inflammatory immune cells, and may influence disease progression through the regulation of inflammatory immune signaling pathway. A new prognostic prediction model for IPF based on PRDEGs was successfully developed.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"143 ","pages":"Article 113572"},"PeriodicalIF":4.8,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604001","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":"Complement C1S is a potential prognostic biomarker and associated with M2 macrophage infiltration in gliomas: From bioinformatics to comprehensive experimental validation","authors":"Lun Gao ,&nbsp;Xiongfei Jing ,&nbsp;Qiuwei Hua ,&nbsp;Zhiyang Li ,&nbsp;Pan Lei ,&nbsp;Ping Song ,&nbsp;Long Zhou ,&nbsp;Yihao Tian ,&nbsp;Junhui Liu ,&nbsp;Qiang Cai","doi":"10.1016/j.intimp.2024.113573","DOIUrl":"10.1016/j.intimp.2024.113573","url":null,"abstract":"<div><div>Glioma is the most common malignant tumor of the central nervous system, and the ability of traditional clinical treatment to prolong the survival of glioma patients is limited. A substantial body of evidence underscores the pivotal role of the immune system in eradicating malignant cells and impeding tumor metastasis. Consequently, tumor immunotherapy has become a promising avenue to address the clinical conundrum faced by glioma patients. The complement system is a natural immune system that is an important line of defense in the immune response. C1S plays a key role in activating the classical complement system. Nevertheless, few studies have focused on the role of C1S in glioma tumorigenesis and progression. In this study, we demonstrated that C1S was upregulated in GBM (Grade IV) and low-grade gliomas (LGG, Grade II-III) by combining glioma cohorts from multiple public databases with our internal independent cohorts and that increased C1S expression levels predict a poor prognosis for gliomas. Cox regression analysis identified C1S as an important prognostic indicator for glioma patients. In addition, gene functional enrichment analysis demonstrated that C1S was involved in cellular immunity, T-cell activation, macrophage differentiation, and cell proliferation. Further experiments demonstrated that C1S facilitates tumor cell proliferation, cell migration and intracranial tumor growth in nude mice. More importantly, we evaluated the role of C1S in immune infiltration. These results suggested that C1S was closely related to a variety of immune cell types in glioma, especially M2 macrophages. Our findings were further validated via glioma tissue microarray immunohistochemical analysis and an M2 macrophage infiltration assay. Together, these findings revealed the underlying critical role of C1S in glioma tumorigenesis, progression, and the tumor immune microenvironment, contributing to further understanding of glioma pathogenesis and guiding immunotherapy.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"143 ","pages":"Article 113573"},"PeriodicalIF":4.8,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603993","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 \"Combined sulforaphane and β-sitosterol mitigate against olanzapine-induced metabolic disorders in rats: Insights on FOXO, PI3K/AKT, JAK/STAT3, and MAPK signaling pathways\" [Int. Immunopharmacol. 140 (2024) 112904].","authors":"Ehab A M El-Shoura, Lobna A Abdelzaher, Nesreen I Mahmoud, Omar A Farghaly, Mostafa Sabry, Mary Girgis Shahataa, Esraa A Salem, Hebatallah M Saad, Omnya Elhussieny, Magy R Kozman, Ahmed M Atwa","doi":"10.1016/j.intimp.2024.113556","DOIUrl":"https://doi.org/10.1016/j.intimp.2024.113556","url":null,"abstract":"","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":" ","pages":"113556"},"PeriodicalIF":4.8,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619434","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}