Immune Network最新文献_第5页

Aging Mediates Inflammatory Transformation of Kidney-Resident Macrophages via Thrombospondin-1 Signaling. 衰老通过血小板反应蛋白-1信号介导肾巨噬细胞的炎症转化。

IF 4.1 4区医学

Immune Network Pub Date : 2025-11-10 eCollection Date: 2025-12-01 DOI: 10.4110/in.2025.25.e39

Chaelin Kang, Donghwan Yun, Boyoun Jang, Yongjun Kim, Minki Hong, Juhyeon Hwang, Haein Yoon, Jeongmin Oh, Hyun Mu Shin, Kyung Chul Moon, Dong-Sup Lee, Yon Su Kim, Hyun Je Kim, Seung Seok Han

{"title":"Aging Mediates Inflammatory Transformation of Kidney-Resident Macrophages via Thrombospondin-1 Signaling.","authors":"Chaelin Kang, Donghwan Yun, Boyoun Jang, Yongjun Kim, Minki Hong, Juhyeon Hwang, Haein Yoon, Jeongmin Oh, Hyun Mu Shin, Kyung Chul Moon, Dong-Sup Lee, Yon Su Kim, Hyun Je Kim, Seung Seok Han","doi":"10.4110/in.2025.25.e39","DOIUrl":"10.4110/in.2025.25.e39","url":null,"abstract":"Kidney-resident macrophages (KRMs) are long-lived immune cells crucial for maintaining kidney homeostasis, with roles that vary depending on kidney condition. Their phenotypes can exert different effects on kidney status, but how the phenotypes of KRMs evolve in aged kidneys and the resulting impacts on kidney homeostasis remain poorly understood. Through single-cell RNA sequencing, we identified a phenotypic shift in KRMs within aged kidneys characterized by increased oxidative phosphorylation (OXPHOS), which stemmed from crosstalk with surrounding tubules. Among these interactions, thrombospondin-1 (THBS1), derived from tubules, has emerged as a pivotal factor driving OXPHOS in KRMs. Experiments confirmed that THBS1 increased OXPHOS in cultured macrophages, polarizing them toward an inflammatory phenotype marked by the production of IL-1β and IL-10. This shift contributes to the inflammatory state of aged kidneys. Finally, we validated these findings in human kidney tissues from elderly individuals. In conclusion, aged kidneys harbor phenotypically altered KRMs that promote an inflammatory microenvironment, with THBS1 playing a central role in this process. These results underscore the importance of exploring therapeutic strategies targeting this pathway to mitigate the inflammatory shift in aged kidneys.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"25 6","pages":"e39"},"PeriodicalIF":4.1,"publicationDate":"2025-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12780144/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145951191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Virus-like Particle Vaccines Containing RSV Fusion Protein Cleavage Mutations Are Immunogenic and Protective in Cotton Rats With a Prime Dose. 含有RSV融合蛋白裂解突变的病毒样颗粒疫苗在棉大鼠中具有免疫原性和保护性。

IF 4.1 4区医学

Immune Network Pub Date : 2025-10-15 eCollection Date: 2025-10-01 DOI: 10.4110/in.2025.25.e37

Hye Suk Hwang, Young-Man Kwon, Ki-Hye Kim, Young-Tae Lee, Eun-Ju Ko, Arun Meas, Sang-Moo Kang

{"title":"Virus-like Particle Vaccines Containing RSV Fusion Protein Cleavage Mutations Are Immunogenic and Protective in Cotton Rats With a Prime Dose.","authors":"Hye Suk Hwang, Young-Man Kwon, Ki-Hye Kim, Young-Tae Lee, Eun-Ju Ko, Arun Meas, Sang-Moo Kang","doi":"10.4110/in.2025.25.e37","DOIUrl":"10.4110/in.2025.25.e37","url":null,"abstract":"An effective respiratory syncytial virus (RSV) vaccine should elicit neutralizing Abs and confer protection without causing vaccine-enhanced disease. Virus-like particle (VLP) is a safe vaccine platform that can display multivalent Ags similar to a virus and induce potent neutralizing Abs without adjuvant. We investigated the impact of mutations in the furin cleavage site, fusion (F) peptide, and change in the transmembrane (TM) domain of RSV F protein in VLPs on inducing RSV neutralizing Abs and efficacy in a cotton rat model. Palivizumab-binding antigenic site II epitope was preferentially exposed by combination mutations in the furin cleavage sites and F peptide together with a change in the TM domain. A single dose of mutant F protein VLP containing these combination mutations effectively induced IgG Ab responses to post-F and pre-F proteins, neutralizing activities, and protection without apparent lung histopathology. The VLP also induced the highest level of INF-γ, indicating the Th1-skewed immune response against the virus infection. A single dose of RSV F mutant exposing an antigenic site II on VLP vaccine could induce RSV-neutralizing Abs, conferring protection without causing vaccine-enhanced disease in cotton rats.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"25 5","pages":"e37"},"PeriodicalIF":4.1,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12599432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145495417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Unlocking IL-33: New Insights into Tumor Immunity. 解锁IL-33：肿瘤免疫的新见解

IF 4.1 4区医学

Immune Network Pub Date : 2025-10-15 eCollection Date: 2025-10-01 DOI: 10.4110/in.2025.25.e36

Byeong Hoon Kang, Heung Kyu Lee

引用次数: 0

Comprehensive Analysis of scRNA-Seq and Bulk RNA-Seq Identified TIMP1 as a Prognostic Marker in Colorectal Cancer. scRNA-Seq和Bulk RNA-Seq的综合分析发现TIMP1是结直肠癌的预后标志物。

IF 4.1 4区医学

Immune Network Pub Date : 2025-10-15 eCollection Date: 2025-10-01 DOI: 10.4110/in.2025.25.e38

Qian-Wen Luo, Yuan-Chao Shi, Wang-Qiang Jia, Xiao-Hai Zhou, Zheng-Rong Yang, Yan Wang, Quan-Lin Guan

{"title":"Comprehensive Analysis of scRNA-Seq and Bulk RNA-Seq Identified TIMP1 as a Prognostic Marker in Colorectal Cancer.","authors":"Qian-Wen Luo, Yuan-Chao Shi, Wang-Qiang Jia, Xiao-Hai Zhou, Zheng-Rong Yang, Yan Wang, Quan-Lin Guan","doi":"10.4110/in.2025.25.e38","DOIUrl":"10.4110/in.2025.25.e38","url":null,"abstract":"Colorectal cancer (CRC), one of the most prevalent and lethal malignancies of digestive system, continues to impose a substantial burden on global health due to its high morbidity and mortality. Tumor microenvironment (TME) is a critical regulator for CRC progression and therapeutic response, but the in-depth understanding on the relationship of TME with CRC remains to be elucidated. In this study, we leveraged single-cell RNA sequencing (scRNA-seq) and bulk RNA-seq data to dissect the immune heterogeneity in CRC patients. The differential expression genes analysis, functional enrichment analysis, random forest analysis and the Least Absolute Shrinkage and Selection Operator method were used to construct a molecular immune prognostic model. The molecular model demonstrated robust performance in stratifying patients based on their immune microenvironment characteristics. The experimental results showed that TIMP1 was highly expressed in CRC. Knockdown of TIMP1 gene significantly inhibited RKO cell proliferation and invasion. By integrating scRNA-seq and bulk RNA-seq data, we developed a new prognostic model that effectively predicts clinical outcomes in patients with CRC and identifies TIMP1 as a promising prognostic biomarker for CRC.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"25 5","pages":"e38"},"PeriodicalIF":4.1,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12599420/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145495438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Intestinal Dysbiosis Caused by Epithelial Fabp6 Gene Disruption Exacerbates Gut Inflammatory Disease. 上皮Fabp6基因破坏引起的肠道生态失调加剧了肠道炎症性疾病。

IF 5.9 4区医学

Immune Network Pub Date : 2025-10-14 eCollection Date: 2025-10-01 DOI: 10.4110/in.2025.25.e35

Kyeongeun Kwon, Minyoung Kim, Youngrak Jung, Mi Young Yoon, June-Yong Lee, Sang Sun Yoon, Mina Rho, Youn Wook Chung, Ji-Hwan Ryu

{"title":"Intestinal Dysbiosis Caused by Epithelial Fabp6 Gene Disruption Exacerbates Gut Inflammatory Disease.","authors":"Kyeongeun Kwon, Minyoung Kim, Youngrak Jung, Mi Young Yoon, June-Yong Lee, Sang Sun Yoon, Mina Rho, Youn Wook Chung, Ji-Hwan Ryu","doi":"10.4110/in.2025.25.e35","DOIUrl":"10.4110/in.2025.25.e35","url":null,"abstract":"Ileal lipid binding protein (Ilbp), encoded by Fabp6 gene, plays a critical role in intracellular transport of bile acids (BAs) from apical to basolateral side of ileal enterocytes, maintaining BA homeostasis within enterohepatic circulation. However, pathophysiological consequences of Ilbp deficiency remain largely unexplored. Here, we demonstrate that disruption of BA balance, caused by intestinal epithelial cell (IEC)-specific Fabp6 gene knockout (Fabp6 ΔIEC), exacerbates dextran sulfate sodium (DSS)-induced gut inflammation. Fecal microbiota transplantation from Fabp6 ΔIEC mice to germ free recipient mice replicated the adverse effects observed in Fabp6 ΔIEC mice, which were mitigated when these mice were co-housed with control (Fabp6 f/f) mice. Metagenomic analysis identified Ligilactobacillus murinus as a primarily diminished strain in Fabp6 ΔIEC mice. Oral administration of L. murinus isolated from feces of Fabp6 f/f mice ameliorated DSS-induced colitis in Fabp6 ΔIEC mice by restoring epithelial barrier integrity and lowering pro-inflammatory cytokines IL-1β, IL-6 and TNF-α. Furthermore, daily administration of taurodeoxycholic acid-one of the BAs reduced in Fabp6 ΔIEC mice and that promotes the growth of L. murinus in an in vitro growth assay-also exhibited a protective effect against DSS-induced colitis through a similar mechanism. These findings suggest that deficiency of specific BAs due to epithelial Fabp6 deletion leads to gut dysbiosis, predisposing the host to inflammatory disease.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"25 5","pages":"e35"},"PeriodicalIF":5.9,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12599461/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145495385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

IL-22 Exacerbates Coxsackievirus Type B3-Induced Pancreatitis by Elevating Viral Replication Through STAT3 Activation. IL-22通过STAT3激活提高病毒复制，加重柯萨奇病毒b3型诱导的胰腺炎

IF 4.1 4区医学

Immune Network Pub Date : 2025-09-01 eCollection Date: 2025-10-01 DOI: 10.4110/in.2025.25.e34

Dae-Joon Kim, Jae-Hyoung Song, Jae-Hyeon Jeong, Jae-Hee Ahn, Jaewon Cho, Seo-Hyeon Mun, Eun-Hye Hong, Sungchan Cho, Sun-Young Chang, Dae Hee Kim, Hyun-Jeong Ko

{"title":"IL-22 Exacerbates Coxsackievirus Type B3-Induced Pancreatitis by Elevating Viral Replication Through STAT3 Activation.","authors":"Dae-Joon Kim, Jae-Hyoung Song, Jae-Hyeon Jeong, Jae-Hee Ahn, Jaewon Cho, Seo-Hyeon Mun, Eun-Hye Hong, Sungchan Cho, Sun-Young Chang, Dae Hee Kim, Hyun-Jeong Ko","doi":"10.4110/in.2025.25.e34","DOIUrl":"10.4110/in.2025.25.e34","url":null,"abstract":"Coxsackievirus type B3 (CVB3) is implicated in diseases such as chronic myocarditis and pancreatitis. While IL-22 is known to play complex roles in immune responses during viral infections, its role in CVB3-induced pancreatitis remains unclear. This study examined the impact of IL-22 on pancreatic pathology during CVB3 infection using histological analyses, glucose tolerance tests, immunostaining, viral load quantification, and molecular assays in both mouse pancreatic tissues and HeLa cells. The results demonstrate that IL-22 exacerbates CVB3-induced pancreatitis by promoting viral replication and pancreatic injury. Mechanistically, IL-22 enhances CVB3 replication through recruitment of phosphatidylinositol 4-kinase III beta, mediated by STAT3 activation. These findings reveal a detrimental role for IL-22 in CVB3 infection, characterized by increased apoptosis, β-cell dysfunction, and elevated viral load, providing new insight into the pathogenesis of virus-induced pancreatitis.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"25 5","pages":"e34"},"PeriodicalIF":4.1,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12599472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145495402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TXNIP Suppresses Lung Cancer Progression by Inhibiting TRAF6-Mediated NF-κB Activation and Autophagy. TXNIP通过抑制traf6介导的NF-κB活化和自噬抑制肺癌进展。

IF 4.1 4区医学

Immune Network Pub Date : 2025-09-01 eCollection Date: 2025-10-01 DOI: 10.4110/in.2025.25.e33

Ji Young Kim, Mi-Jeong Kim, Ji Hye Shin, Kyung-Hwa Baik, Yeeun Kang, Yoolim Sung, Seo Hyun Kim, Ha-Jeong Lee, Chaeeun Lee, Jae-Hyuck Shim, Duk-Hwan Kim, Eunyoung Chun, Ki-Young Lee

{"title":"TXNIP Suppresses Lung Cancer Progression by Inhibiting TRAF6-Mediated NF-κB Activation and Autophagy.","authors":"Ji Young Kim, Mi-Jeong Kim, Ji Hye Shin, Kyung-Hwa Baik, Yeeun Kang, Yoolim Sung, Seo Hyun Kim, Ha-Jeong Lee, Chaeeun Lee, Jae-Hyuck Shim, Duk-Hwan Kim, Eunyoung Chun, Ki-Young Lee","doi":"10.4110/in.2025.25.e33","DOIUrl":"10.4110/in.2025.25.e33","url":null,"abstract":"Thioredoxin-interacting protein (TXNIP) functions as a tumor suppressor, but its role in lung cancer remains poorly defined. This study identifies TXNIP as a negative regulator of TNF receptor-associated factor 6 (TRAF6)-mediated NF-κB activation and autophagy, key pathways in tumor progression. TXNIP directly binds TRAF6 via its C-terminal arrestin domain, inhibiting TRAF6 dimerization and auto-ubiquitination. This, in turn, reduces ubiquitination of downstream targets TGF-β-activated kinase 1 and beclin 1 (BECN1), thereby suppressing NF-κB signaling and autophagic activity. TXNIP expression is significantly reduced in lung adenocarcinoma and lung squamous cell carcinoma, as demonstrated by public datasets and patient tissue analysis. Gene set enrichment analysis shows that non-small cell lung cancer patients with TXNIPDOWN and TRAF6UP expression exhibit increased metastasis-associated gene signatures and poorer survival outcomes. Functionally, TXNIP-knockout lung cancer cells show enhanced TRAF6 and BECN1 ubiquitination, increased LC3 puncta, and elevated NF-κB activity and cytokine production after TLR3/4 stimulation. These cells also display increased proliferation, migration, invasion, and colony formation in vitro across multiple lung cancer cell lines (A549 and H1299). Collectively, this study highlights TXNIP as a critical suppressor of TRAF6-driven oncogenic pathways in lung cancer, suggesting that its downregulation contributes to disease progression through enhanced TLR-induced signaling.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"25 5","pages":"e33"},"PeriodicalIF":4.1,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12599409/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145495434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Enigmatic Roles of Complement Anaphylatoxin Signaling in Health and Disease. 补体过敏毒素信号在健康和疾病中的神秘作用。

IF 5.9 4区医学

Immune Network Pub Date : 2025-08-20 eCollection Date: 2025-08-01 DOI: 10.4110/in.2025.25.e32

Anthony Shadid, Kathryn D Hok, Aleksey Y Domozhirov, Tingting Weng-Mills, Marie-Françoise Doursout, Nirmal K Banda, Marcos I Restrepo, Pooja Shivshankar

{"title":"Enigmatic Roles of Complement Anaphylatoxin Signaling in Health and Disease.","authors":"Anthony Shadid, Kathryn D Hok, Aleksey Y Domozhirov, Tingting Weng-Mills, Marie-Françoise Doursout, Nirmal K Banda, Marcos I Restrepo, Pooja Shivshankar","doi":"10.4110/in.2025.25.e32","DOIUrl":"10.4110/in.2025.25.e32","url":null,"abstract":"Complement anaphylatoxins C3a and C5a are potent immunomodulators whose impact extends well beyond their traditional roles in innate immunity. Acting through G protein-coupled receptors C3aR, C5aR1, and C5aR2, these peptides take part in coordinating immune cell recruitment, vascular tone, and tissue remodeling. Yet their functions are deeply context-dependent: while they play essential roles in microbial clearance and immune coordination, their overactivation contributes to immunopathology in a wide range of diseases. The anaphylatoxins play key roles in early pathogen containment but can also drive cytokine storm and tissue damage, as in coronavirus disease 2019 (COVID-19) and bacterial sepsis. In autoimmune conditions, the anaphylatoxins promote leukocyte infiltration and complement-mediated tissue injury. In chronic diseases, they contribute to fibrosis in diabetic kidney disease and idiopathic pulmonary fibrosis, and anaphylatoxins disrupt neurovascular integrity in neurodegenerative diseases. In cancer, C3a and C5a shape the tumor microenvironment by facilitating immune evasion, angiogenesis, and metastasis. As complement-targeted therapies gain momentum in clinical settings-particularly in the treatment of genetic disorders, such as paroxysmal nocturnal hemoglobinuria, more recently COVID-19, and cancer-a deeper mechanistic understanding of C3a and C5a signaling is imperative as we advance closer toward precision medicine, and this review aims to inform future approaches for therapeutic complement modulation.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"25 4","pages":"e32"},"PeriodicalIF":5.9,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12411103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Does the Single Nucleotide Polymorphism rs2228145 in IL6R Truly Reflect IL-6 Signaling in Mendelian Randomization Studies? 孟德尔随机化研究中il - 6r单核苷酸多态性rs2228145是否真实反映IL-6信号？

IF 4.1 4区医学

Immune Network Pub Date : 2025-08-18 eCollection Date: 2025-08-01 DOI: 10.4110/in.2025.25.e31

Mengyi Zhu, Minghui Cao, Liling Lin

引用次数: 0

Arginine Metabolism in Cancer Biology and Immunotherapy. 精氨酸代谢在肿瘤生物学和免疫治疗中的应用。

IF 4.1 4区医学

Immune Network Pub Date : 2025-08-12 eCollection Date: 2025-08-01 DOI: 10.4110/in.2025.25.e30

DingYuan Bai, YuXuan Zhou, LingJie Jing, Cheng Guo, QuanJun Yang

引用次数: 0