Immune Network最新文献_第7页

SiglecF Expressing Neutrophils Exacerbate Th17-Mediated Autoimmune Neuroinflammation. 表达中性粒细胞SiglecF加剧th17介导的自身免疫性神经炎症。

IF 4.3 4区医学

Immune Network Pub Date : 2025-04-14 eCollection Date: 2025-06-01 DOI: 10.4110/in.2025.25.e19

Wonseok Hu, Leezhi Kwon, Yu Sun Jeong, Geon Ho Bae, Ye Seon Kim, Brian A Zabel, Yoe-Sik Bae

{"title":"SiglecF Expressing Neutrophils Exacerbate Th17-Mediated Autoimmune Neuroinflammation.","authors":"Wonseok Hu, Leezhi Kwon, Yu Sun Jeong, Geon Ho Bae, Ye Seon Kim, Brian A Zabel, Yoe-Sik Bae","doi":"10.4110/in.2025.25.e19","DOIUrl":"10.4110/in.2025.25.e19","url":null,"abstract":"Multiple sclerosis is an autoimmune disease characterized by numerous immune cells, including neutrophils, infiltrating the central nervous system. Previous reports point to a complex role for neutrophils in experimental autoimmune encephalomyelitis (EAE), where their heterogeneity remains poorly understood. In this study, we identified a unique population of neutrophils expressing SiglecF in the brain during EAE that can influence T cell activity. These neutrophils produced elevated levels of Th17-polarizing cytokines, including IL-6, IL-1β, IL-23, and TNF-α, both in vivo and in vitro. Consistent with this cytokine profile, co-culturing SiglecF+ neutrophils with CD4+ T cells promoted Th17 and GM-CSF+ pathogenic Th17 differentiation and proliferation while reducing regulatory T cell numbers. Depleting SiglecF+ neutrophils with anti-SiglecF Abs reduced the severity of EAE, decreased the Th17 population, and increased the regulatory T cell population in the brain. These findings suggest that SiglecF+ neutrophils promote autoimmune neuroinflammation by reinforcing pathogenic autoreactive Th17 cell responses.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"25 3","pages":"e19"},"PeriodicalIF":4.3,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575393","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

Cytokines in Focus: IL-2 and IL-15 in NK Adoptive Cell Cancer Immunotherapy. 细胞因子的焦点：IL-2和IL-15在NK过继细胞癌免疫治疗中的作用。

IF 4.3 4区医学

Immune Network Pub Date : 2025-04-09 eCollection Date: 2025-04-01 DOI: 10.4110/in.2025.25.e17

Bryan Marr, Donghyeon Jo, Mihue Jang, Seung-Hwan Lee

引用次数: 0

Novel STAT3 Y360C Gain-of-function Variant Underlies Immune Dysregulation and Aberrancy in Mitochondrial Dynamics. 新的STAT3 Y360C功能获得变异是线粒体动力学免疫失调和异常的基础。

IF 4.3 4区医学

Immune Network Pub Date : 2025-04-09 eCollection Date: 2025-04-01 DOI: 10.4110/in.2025.25.e18

Kornvalee Meesilpavikkai, Kasiphak Kaikaew, Zijun Zhou, Virgil A S H Dalm, Fabian M P Kaiser, Christopher Schliehe, Sigrid M A Swagemakers, Peter J van der Spek, Benjamin Schrijver, Pamela Vasic, Maaike de Bie, Marleen Bakker, Chiara Milanese, Pier G Mastroberardino, Nattiya Hirankarn, Narissara Suratannon, Hanna IJspeert, Willem A Dik, P Martin van Hagen

{"title":"Novel STAT3 Y360C Gain-of-function Variant Underlies Immune Dysregulation and Aberrancy in Mitochondrial Dynamics.","authors":"Kornvalee Meesilpavikkai, Kasiphak Kaikaew, Zijun Zhou, Virgil A S H Dalm, Fabian M P Kaiser, Christopher Schliehe, Sigrid M A Swagemakers, Peter J van der Spek, Benjamin Schrijver, Pamela Vasic, Maaike de Bie, Marleen Bakker, Chiara Milanese, Pier G Mastroberardino, Nattiya Hirankarn, Narissara Suratannon, Hanna IJspeert, Willem A Dik, P Martin van Hagen","doi":"10.4110/in.2025.25.e18","DOIUrl":"https://doi.org/10.4110/in.2025.25.e18","url":null,"abstract":"The STAT3 is an important regulator in a wide range of different cell types. Human STAT3 variants are associated with several immune dysregulation diseases. The current study investigated the clinical, genetic, and immunobiological data obtained from a family with novel heterozygous STAT3 variants located at p.Y360C of the DNA binding domain. The clinical manifestations of these patients include autoimmunity, immunodeficiency, and postnatal growth defects. Broad STAT3 regulated cells including patient primary immune cells and HEK293 cells harboring the variant were assessed. Remarkably high levels of STAT3-regulated cytokines were detected in the sera of the patients. STAT3 nuclear binding and STAT3 activity were higher in STAT3-transduced HEK293 cells containing the p.Y360C variant when compared to HEK cells expressing wild type (WT) STAT3. Upon cytokine activation, STAT3 variants inhibited nuclear translocation of the WT STAT3 molecule. We also demonstrated that PBMCs from these patients exhibit significantly higher mitochondrial activity compared to that of healthy controls. The exploration of the effects of STAT3 Y360C variants described in our study provides novel insights into the molecular effects of the STAT3 variant and its role in the pathophysiology of STAT3 gain-of-function syndromes.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"25 2","pages":"e18"},"PeriodicalIF":4.3,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12056293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144010707","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

Succinate Dehydrogenase Regulates Homeostasis and Metabolic Integrity of Alveolar Macrophages. 琥珀酸脱氢酶调节肺泡巨噬细胞的稳态和代谢完整性。

IF 4.3 4区医学

Immune Network Pub Date : 2025-04-08 eCollection Date: 2025-06-01 DOI: 10.4110/in.2025.25.e16

Seung Geun Song, Ein Lee, Jaemoon Koh, Doo Hyun Chung

{"title":"Succinate Dehydrogenase Regulates Homeostasis and Metabolic Integrity of Alveolar Macrophages.","authors":"Seung Geun Song, Ein Lee, Jaemoon Koh, Doo Hyun Chung","doi":"10.4110/in.2025.25.e16","DOIUrl":"10.4110/in.2025.25.e16","url":null,"abstract":"Lung tissue-resident macrophages, including alveolar macrophages (AMs) and interstitial macrophages (IMs), are pivotal in maintaining both immune defense and tissue homeostasis. Although the distinct functional roles of these macrophage populations are well recognized, the specific metabolic pathways that support their functions are not fully understood. Comparative RNA sequencing analysis identified Sdha, a key enzyme in mitochondrial metabolism, as one of the most highly expressed and differentially regulated genes involved in metabolic pathways in AMs relative to IMs. This finding led us to investigate the role of succinate dehydrogenase complex subunit A (SDHA) in regulating AM metabolism and function. Here, we demonstrated that SDHA is crucial for maintaining AM homeostasis. Deletion of SDHA resulted in a significant reduction in AM populations without affecting IMs, highlighting an AM-specific requirement for SDHA. In the absence of SDHA, AMs underwent metabolic reprogramming towards glycolysis compared with IMs, along with significant transcriptional changes and cell death. Furthermore, SDHA-deficient AMs showed lipid accumulation and increased endoplasmic reticulum stress. These findings establish SDHA as a crucial regulator of AM metabolism and underscore the importance of maintaining metabolic integrity for AM function and survival within the lung microenvironment.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"25 3","pages":"e16"},"PeriodicalIF":4.3,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226257/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575396","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

Regulatory T Cell Metabolism: A Promising Therapeutic Target for Cancer Treatment? 调节性T细胞代谢：一个有希望的癌症治疗靶点？

IF 4.3 4区医学

Immune Network Pub Date : 2025-02-24 eCollection Date: 2025-02-01 DOI: 10.4110/in.2025.25.e13

Jihyoun Kim, Jiaoran Li, Jun Wei, Seon Ah Lim

{"title":"Regulatory T Cell Metabolism: A Promising Therapeutic Target for Cancer Treatment?","authors":"Jihyoun Kim, Jiaoran Li, Jun Wei, Seon Ah Lim","doi":"10.4110/in.2025.25.e13","DOIUrl":"10.4110/in.2025.25.e13","url":null,"abstract":"Regulatory T (Treg) cells are essential for maintaining immune homeostasis by suppressing excessive immune responses. In the context of cancer, however, Tregs promote immune evasion and tumor progression, particularly through their unique adaptations within the tumor microenvironment (TME). Recent research has emphasized how metabolic characteristics shape Treg activation, migration, and immunosuppressive function, revealing the impact of metabolic pathways on Treg fitness in homeostasis and within the TME. In this review, we first provide an overview of Tregs in cancer immunology, discussing their immunosuppressive roles and properties specific to the TME. We then examine the metabolic requirements for Treg activation and migration under normal conditions, followed by a discussion of how hypoxia, lactate accumulation, nutrient limitation, oxidative stress, and other TME-specific factors alter Treg metabolism and contribute to cancer immune evasion. Finally, we explore therapeutic strategies that target Treg metabolism within the TME, including pharmacological modulation of specific metabolic pathways to diminish Treg-mediated immunosuppression. Thus, we could suggest future directions and clinical implications for Treg-targeted metabolic modulation as a complementary approach in cancer treatment, setting the stage for novel strategies in immunotherapy.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"25 1","pages":"e13"},"PeriodicalIF":4.3,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11896657/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614803","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

Modulation of Immune Responses by Metabolic Reprogramming: The Key Role of Immunometabolism. 代谢重编程对免疫反应的调节：免疫代谢的关键作用。

IF 4.1 4区医学

Immune Network Pub Date : 2025-02-24 eCollection Date: 2025-02-01 DOI: 10.4110/in.2025.25.e15

Sung-Gyoo Park, June-Yong Lee, Hyungseok Seo, Soo Seok Hwang, Chong-Kil Lee, Gap Ryol Lee

引用次数: 0

Metabolic Signaling as a Driver of T Cell Aging. 代谢信号作为T细胞衰老的驱动因素。

IF 4.3 4区医学

Immune Network Pub Date : 2025-02-24 eCollection Date: 2025-02-01 DOI: 10.4110/in.2025.25.e14

Minju Choi, Sujin Choi, Minkyeong Cho, Chulwoo Kim

引用次数: 0

Diverse Functions of Macrophages in Obesity and Metabolic Dysfunction-Associated Steatotic Liver Disease: Bridging Inflammation and Metabolism. 巨噬细胞在肥胖和代谢功能障碍相关的脂肪变性肝病中的多种功能：桥接炎症和代谢

IF 4.3 4区医学

Immune Network Pub Date : 2025-02-21 eCollection Date: 2025-02-01 DOI: 10.4110/in.2025.25.e12

Jun Hee Jang, Jin Hyun Sung, Jin Young Huh

{"title":"Diverse Functions of Macrophages in Obesity and Metabolic Dysfunction-Associated Steatotic Liver Disease: Bridging Inflammation and Metabolism.","authors":"Jun Hee Jang, Jin Hyun Sung, Jin Young Huh","doi":"10.4110/in.2025.25.e12","DOIUrl":"10.4110/in.2025.25.e12","url":null,"abstract":"Macrophages play crucial roles in immune response and tissue homeostasis, with their functions becoming increasingly complex in obesity-mediated metabolic disorders. This review explores the extensive range of macrophage activities within adipose and liver tissues, emphasizing their contribution to the pathogenesis and progression of obesity and its related metabolic dysfunction-associated steatotic liver disease (MASLD). In the context of obesity, macrophages respond adaptively to lipid overloads and inflammatory cues in adipose tissue, profoundly influencing insulin resistance and metabolic homeostasis. Concurrently, their role in the liver extends to moderating inflammation and orchestrating fibrotic responses, integral to the development of MASLD. Highlighting the spectrum of macrophage phenotypes across these metabolic landscapes, we summarize their diverse roles in linking inflammatory processes with metabolic functions. This review advocates for a deeper understanding of macrophage subsets in metabolic tissues, proposing targeted research to harness their therapeutic potential in mitigating MASLD and other metabolic disorders.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"25 1","pages":"e12"},"PeriodicalIF":4.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11896663/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614827","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

Regulation of Adaptive Immunity by Lipid Post-translational Modifications. 脂质翻译后修饰对适应性免疫的调节

IF 4.3 4区医学

Immune Network Pub Date : 2025-02-18 eCollection Date: 2025-02-01 DOI: 10.4110/in.2025.25.e11

Jonathan R Mattingly, Aimee Wu, Autumn G York

引用次数: 0

Mitochondrial Regulator CRIF1 Plays a Critical Role in the Development and Homeostasis of Alveolar Macrophages via Maintaining Metabolic Fitness. 线粒体调节因子CRIF1通过维持代谢适应度在肺泡巨噬细胞的发育和稳态中发挥关键作用。

IF 4.3 4区医学

Immune Network Pub Date : 2025-02-14 eCollection Date: 2025-02-01 DOI: 10.4110/in.2025.25.e9

Ein Lee, Seung Geun Song, Haaun Moon, Minho Shong, Doo Hyun Chung

{"title":"Mitochondrial Regulator CRIF1 Plays a Critical Role in the Development and Homeostasis of Alveolar Macrophages via Maintaining Metabolic Fitness.","authors":"Ein Lee, Seung Geun Song, Haaun Moon, Minho Shong, Doo Hyun Chung","doi":"10.4110/in.2025.25.e9","DOIUrl":"10.4110/in.2025.25.e9","url":null,"abstract":"The importance of mitochondrial function in macrophages is well established. Alveolar macrophages (AMs), the tissue-resident macrophages (TRMs) of the lung, are particularly dependent on mitochondria-driven oxidative phosphorylation (OXPHOS) to support their functions and maintain homeostasis. However, the specific genes and pathways that regulate OXPHOS in AMs remain unclear. In this study, we investigated the role of CR6-interacting factor 1 (CRIF1), a mitochondrial regulator, as a key factor that specifically modulates the metabolic fitness and maintenance of AMs. Using single-cell RNA sequencing and transcriptomic analyses, we found CRIF1 to be highly expressed in AMs compared to TRMs from other tissues, correlating with enhanced OXPHOS activity. Genetic ablation of Crif1 in macrophages resulted in a marked reduction in AM populations exclusively in the lung, while other TRM populations were unaffected. CRIF1-deficient AMs exhibited an altered metabolic profile, including impaired mitochondrial function, increased glycolysis, and aberrant lipid accumulation. These findings underscore the essential role of CRIF1 in regulating mitochondrial functions and metabolic fitness in AMs, distinguishing it from broader mitochondrial regulators like mitochondrial transcription factor A, which operates across multiple TRM populations. Our study provides critical insights into the tissue-specific regulation of macrophage metabolism and suggests potential therapeutic avenues for lung diseases associated with AM dysfunction.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"25 1","pages":"e9"},"PeriodicalIF":4.3,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11896662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614833","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