International Reviews of Immunology最新文献

Retraction. 撤回。

IF 4.3 4区医学

International Reviews of Immunology Pub Date : 2024-11-11 DOI: 10.1080/08830185.2024.2423548

引用次数: 0

Retraction. 撤回。

IF 4.3 4区医学

International Reviews of Immunology Pub Date : 2024-11-11 DOI: 10.1080/08830185.2024.2423553

引用次数: 0

Recurrent respiratory papillomatosis: Immunological mechanisms involved in recurrence. 复发性呼吸道乳头状瘤病：复发的免疫机制。

IF 5.4 4区医学

International Reviews of Immunology Pub Date : 2024-11-07 DOI: 10.1080/08830185.2024.2425428

Katya Karen López-Aguilar, María Eugenia Vargas-Camaño, Fernando Lozano-Patiño, María Isabel Castrejón Vázquez

引用次数: 0

The NLRP3 inflammasome: Mechanisms of activation, regulation, and role in diseases. NLRP3 炎症小体：激活机制、调控和在疾病中的作用。

IF 4.3 4区医学

International Reviews of Immunology Pub Date : 2024-10-14 DOI: 10.1080/08830185.2024.2415688

Mina Dadkhah, Mohammadreza Sharifi

引用次数: 0

Transforming growth factor-β in tumor microenvironment: Understanding its impact on monocytes and macrophages for its targeting. 肿瘤微环境中的转化生长因子-β：了解其对单核细胞和巨噬细胞的影响，以实现靶向治疗。

IF 4.3 4区医学

International Reviews of Immunology Pub Date : 2024-10-08 DOI: 10.1080/08830185.2024.2411998

Tetiana Hourani, Amit Sharma, Rodney B Luwor, Adrian A Achuthan

引用次数: 0

FUNDC1 mediated mitochondria-dependent ferroptosis of epithelial cells in model of asthma by FBXL2/ar/GPX4 signaling pathway of SUMO1 at K136. FUNDC1 通过 K136 处 SUMO1 的 FBXL2/ar/GPX4 信号通路介导哮喘模型中上皮细胞的线粒体依赖性铁氧化。

IF 4.3 4区医学

International Reviews of Immunology Pub Date : 2024-09-25 DOI: 10.1080/08830185.2024.2406853

Li Li, Xingxing Zhu, Jiayi Zhao, Jiaying Yuan, Haoran Ni, Jian Fan, Yi Zhang, Yahong Sun, Yan Shang

{"title":"FUNDC1 mediated mitochondria-dependent ferroptosis of epithelial cells in model of asthma by FBXL2/ar/GPX4 signaling pathway of SUMO1 at K136.","authors":"Li Li, Xingxing Zhu, Jiayi Zhao, Jiaying Yuan, Haoran Ni, Jian Fan, Yi Zhang, Yahong Sun, Yan Shang","doi":"10.1080/08830185.2024.2406853","DOIUrl":"https://doi.org/10.1080/08830185.2024.2406853","url":null,"abstract":"This study aimed to explore the critical role of FUNDC1 on epithelial cells in model of asthma. Patients with asthma and normal healthy volunteers were obtained from our hospital. The serum of FUNDC1 mRNA expression was down-regulated in patients with asthma. Meanwhile, the serum of FUNDC1 mRNA expression was positive correlation with IgE and anti-HDM IgE protein. FUNDC1 expression in lung tissue of mice model was decreased in mice model of asthma. Sh-FUNDC1 enhanced asthma in mice model of asthma. FUNDC1 up-regulation reduced IL-4, IL-5, IL-10 and IL-13 activity levels in vitro model of asthma.FUNDC1 down-regulation promoted IL-4, IL-5, IL-10 and IL-13 activity levels in vitro model of asthma. FUNDC1 reduced ferroptosis of epithelial cells in model of asthma through the inhibition of mitochondrial damage. FUNDC1 induced FBXL2 and AR protein expression in model of asthma. FUNDC1 interlinked with FBXL2 is modified by SUMO1 at K136. FBXL2, ASN-205, GLN-204, ARG-235, and GLN-237 form hydrogen bonds with FUNDC1's ASP-15, ASP-16, GLU-25, and ARG-29, with lengths of 2.3, 3.1, 2.9, 2.3, and 2.9 Å, respectively. The induction of FBXL2 reduced the effects of Sh-FUNDC1 on asthma in mice model of asthma. The inhibition of AR reduced the effects of Sh-FUNDC1 on asthma in mice model of asthma Overall, FUNDC1 prevents ferroptosis of airway epithelial cells of asthma through FBXL2/AR/GPX4 signaling pathway of SUMO1 at K136. FUNDC1 might benefit the treatment of asthma or other pulmonary disease.","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":" ","pages":"1-13"},"PeriodicalIF":4.3,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142346688","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}

引用次数: 0

Re-inventing traditional aluminum-based adjuvants: Insight into a century of advancements. 重新发明传统铝基佐剂：洞察一个世纪的进步。

IF 4.3 4区医学

International Reviews of Immunology Pub Date : 2024-09-23 DOI: 10.1080/08830185.2024.2404095

Himanshu Gogoi, Rajesh Mani, Rakesh Bhatnagar

{"title":"Re-inventing traditional aluminum-based adjuvants: Insight into a century of advancements.","authors":"Himanshu Gogoi, Rajesh Mani, Rakesh Bhatnagar","doi":"10.1080/08830185.2024.2404095","DOIUrl":"https://doi.org/10.1080/08830185.2024.2404095","url":null,"abstract":"Aluminum salt-based adjuvants like alum, alhydrogel and Adju-Phos are by far the most favored clinically approved vaccine adjuvants. They have demonstrated excellent safety profile and currently used in vaccines against diphtheria, tetanus, pertussis, hepatitis B, anthrax etc. These vaccinations cause minimal side effects like local inflammation at the injection site. Aluminum salt-based adjuvants primarily stimulate CD4+ T cells and B cell mediated Th2 immune response leading to generate a robust antibody response. In this review article, we have compiled the role of physio-chemical role of the two commonly used aluminum salt-based adjuvants alhydrogel and Adju-Phos, and the effect of surface properties, buffer composition, and adjuvant dosage on the immune response. After being studied for almost a century, researchers have come up with various mechanism by which these aluminum adjuvants activate the immune system. Firstly, we have covered the initial works of Glenny and his \"repository effect\" which paved the work for his successors to explore the involvement of cytokines, chemokines, recruitment of innate immune cells, enhanced antigen uptake by antigen presenting cells, and formation of NLRP3 inflammasome complex in mediating the immune response. It has been reported that aluminum adjuvants activate multiple immunological pathways which synergistically activates the immune system. We later discuss the recent developments in nanotechnology-based preparations of next generation aluminum based adjuvants which has enabled precise size control and morphology of the traditional aluminum adjuvants thereby manipulating the immune response as per our desire.","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":" ","pages":"1-24"},"PeriodicalIF":4.3,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142287233","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}

引用次数: 0

The m6A methyltransferase METTL3 modifies Kcnk6 promoting on inflammation associated carcinogenesis is essential for colon homeostasis and defense system through histone lactylation dependent YTHDF2 binding. m6A甲基转移酶METTL3通过组蛋白乳酰化依赖性YTHDF2结合，修饰Kcnk6，促进与炎症相关的癌变，对结肠稳态和防御系统至关重要。

IF 5 4区医学

International Reviews of Immunology Pub Date : 2024-09-13 DOI: 10.1080/08830185.2024.2401358

Xiaolong Yuan,Qiong Wang,Jun Zhao,Haitang Xie,Zhichen Pu

{"title":"The m6A methyltransferase METTL3 modifies Kcnk6 promoting on inflammation associated carcinogenesis is essential for colon homeostasis and defense system through histone lactylation dependent YTHDF2 binding.","authors":"Xiaolong Yuan,Qiong Wang,Jun Zhao,Haitang Xie,Zhichen Pu","doi":"10.1080/08830185.2024.2401358","DOIUrl":"https://doi.org/10.1080/08830185.2024.2401358","url":null,"abstract":"Inflammation induces tumor formation and plays a crucial role in tumor progression and prognosis. KCNK6, by regulating K(+) efflux to reduce NLRP3 Inflammasome-induced lung injury, relaxes the aorta. This study aims to elucidate the effects and biological mechanism of KCNK6 in inflammation-associated carcinogenesis, which may be essential for colon homeostasis and the defense system. To induce colitis, mice were given 3.0% Dextran Sodium Sulfate (DSS) in their drinking water for 7 days. The Azoxymethane (AOM) +DSS method was used to induce colon cancer in the mice model. Bone marrow-derived macrophages (BMDM) from Kcnk6-/- mice, AW264.7 cells, and human colon cancer HCT116 and Caco2 cells were used as in vitro models. The loss of Kcnk6 prevented spontaneous colitis and restored mucosal integrity and homeostatic molecules. Additionally, the loss of Kcnk6 reduced the severity of AOM/DSS-induced carcinogenesis. Kcnk6 promoted cell viability and proliferation in HCT-116 or Caco-2 cells. The loss of Kcnk6 inhibited the levels of inflammatory factors in BMDM cells. Kcnk6 accelerated potassium channel activity, inducing NLRP3 inflammasome activation. METTL3-mediated m6A modification increased Kcnk6 stability in a YTHDF2-dependent manner. Histone lactylation activated the transcription of YTHDF2/Kcnk6. Our study revealed the important role of Kcnk6 in inflammation-associated carcinogenesis progression. The m6A methyltransferase METTL3 and histone lactylation increased Kcnk6 stability in a YTHDF2-dependent manner, providing a potential strategy for inflammation-associated carcinogenesis or colorectal cancer therapy.","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":"4 1","pages":"1-16"},"PeriodicalIF":5.0,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142247551","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}

引用次数: 0

Immunometabolism in cancer: A journey into innate and adaptive cells. 癌症中的免疫代谢：先天性和适应性细胞之旅。

IF 4.3 4区医学

International Reviews of Immunology Pub Date : 2024-09-12 DOI: 10.1080/08830185.2024.2401353

Alexia Nedel Sant'Ana, Camila Kehl Dias, Sacha Krolow E Silva, Fabrício Figueiró

{"title":"Immunometabolism in cancer: A journey into innate and adaptive cells.","authors":"Alexia Nedel Sant'Ana, Camila Kehl Dias, Sacha Krolow E Silva, Fabrício Figueiró","doi":"10.1080/08830185.2024.2401353","DOIUrl":"https://doi.org/10.1080/08830185.2024.2401353","url":null,"abstract":"In recent years, mostly spanning the past decade, the concept of immunometabolism has ushered with a novel perspective on carcinogenesis, tumor progression, and tumor response to therapy. It has become clear that the metabolic state of immune cells plays a significant role in shaping their antitumor or protumor activities within the cancer microenvironment. Consequently, the examination of tumor metabolic heterogeneity, including an exploration of immunometabolism, proves indispensable for enhancing prognostic tools and advancing the quest for personalized treatments. Here we have delved into how metabolic reprogramming profoundly influences the acquisition and maintenance of functional states, spanning from effector and cytotoxic profiles to regulatory and immunosuppressive phenotypes in both innate and adaptive immunity. These alterations wield considerable influence over tumor evolution and affect the outcome of cancer. Furthermore, we explore some of the cellular signaling mechanisms that underpin the metabolic and phenotypic flexibility of immune cells in response to external stimuli.","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":" ","pages":"1-14"},"PeriodicalIF":4.3,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142287232","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}

引用次数: 0

The molecular landscape of T cell exhaustion in the tumor microenvironment and reinvigoration strategies. 肿瘤微环境中 T 细胞衰竭的分子图谱和重振策略。

IF 5 4区医学

International Reviews of Immunology Pub Date : 2024-09-11 DOI: 10.1080/08830185.2024.2401352

Mahsa Heidari-Foroozan,Alaleh Rezalotfi,Nima Rezaei

{"title":"The molecular landscape of T cell exhaustion in the tumor microenvironment and reinvigoration strategies.","authors":"Mahsa Heidari-Foroozan,Alaleh Rezalotfi,Nima Rezaei","doi":"10.1080/08830185.2024.2401352","DOIUrl":"https://doi.org/10.1080/08830185.2024.2401352","url":null,"abstract":"Immunotherapy has emerged as a promising therapeutic approach for cancer treatment by harnessing the immune system to target cancer cells. However, the efficacy of immunotherapy is hindered by the tumor microenvironment (TME), comprising regulatory T cells (Tregs), macrophages, myeloid-derived suppressor cells (MDSCs), neutrophils, soluble factors (TGF-β, IL-35, IL-10), and hypoxia. These components interact with inhibitory receptors (IRs) on T cells, leading to alterations in T cell transcriptomes, epigenomes, and metabolism, ultimately resulting in T cell exhaustion and compromising the effectiveness of immunotherapy. T cell exhaustion occurs in two phases: pre-exhaustion and exhaustion. Pre-exhausted T cells exhibit reversibility and distinct molecular properties compared to terminally exhausted T cells. Understanding these differences is crucial for designing effective interventions. This comprehensive review summarizes the characteristics of pre-exhausted and exhausted T cells and elucidates the influence of TME components on T cell activity, transcriptomes, epigenomes, and metabolism, ultimately driving T cell exhaustion in cancer. Additionally, potential intervention strategies for reversing exhaustion are discussed. By gaining insights into the mechanisms underlying T cell exhaustion and the impact of the TME, this review aims to inform the development of innovative approaches for combating T cell exhaustion and enhancing the efficacy of immunotherapy in cancer treatment.","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":"57 1","pages":"1-22"},"PeriodicalIF":5.0,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142185433","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}

引用次数: 0