International Reviews of Immunology最新文献_第2页

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 : 2025-01-01 Epub Date: 2024-10-14 DOI: 10.1080/08830185.2024.2415688

Mina Dadkhah, Mohammadreza Sharifi

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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 : 2025-01-01 Epub Date: 2024-09-12 DOI: 10.1080/08830185.2024.2401353

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

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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 : 2025-01-01 Epub 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":"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":"45-57"},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","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}

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An insight into COVID-19 host immunity at single-cell resolution. 在单细胞分辨率下洞察COVID-19宿主免疫。

IF 4.3 4区医学

International Reviews of Immunology Pub Date : 2024-12-21 DOI: 10.1080/08830185.2024.2443420

Supratim Ghosh, Ankita Chatterjee, Arindam Maitra

引用次数: 0

Can interventions targeting MDSCs improve the outcome of vaccination in vulnerable populations? 针对MDSCs的干预措施能否改善弱势人群的疫苗接种结果？

IF 4.3 4区医学

International Reviews of Immunology Pub Date : 2024-12-21 DOI: 10.1080/08830185.2024.2443423

Yuliya V Perfilyeva, Arthur D Aquino, Maxim A Borodin, Aikyn Kali, Nurshat Abdolla, Yekaterina O Ostapchuk, Raikhan Tleulieva, Anastassiya V Perfilyeva, Nurlan T Jainakbayev, Kamalidin O Sharipov, Nikolai N Belyaev

{"title":"Can interventions targeting MDSCs improve the outcome of vaccination in vulnerable populations?","authors":"Yuliya V Perfilyeva, Arthur D Aquino, Maxim A Borodin, Aikyn Kali, Nurshat Abdolla, Yekaterina O Ostapchuk, Raikhan Tleulieva, Anastassiya V Perfilyeva, Nurlan T Jainakbayev, Kamalidin O Sharipov, Nikolai N Belyaev","doi":"10.1080/08830185.2024.2443423","DOIUrl":"https://doi.org/10.1080/08830185.2024.2443423","url":null,"abstract":"Preventive vaccination is a crucial strategy for controlling and preventing infectious diseases, offering both effectiveness and cost-efficiency. However, despite the widespread success of vaccination programs, there are still certain population groups who struggle to mount adequate responses to immunization. These at-risk groups include but are not restricted to the elderly, overweight individuals, individuals with chronic infections and cancer patients. All of these groups are characterized by persistent chronic inflammation. Recent studies have demonstrated that one of the key players in immune regulation and the promotion of chronic inflammation are myeloid-derived suppressor cells (MDSCs). These cells possess a wide range of immunosuppressive mechanisms and are able to dampen immune responses in both antigen-specific and antigen-nonspecific manner, thus contributing to the establishment and maintenance of an inflammatory environment. Given their pivotal role in immune modulation, there is growing interest in understanding how MDSCs may influence the efficacy of vaccines, particularly in vulnerable populations. In this narrative review, we discuss whether MDSCs are able to regulate vaccine-induced immunity and whether their suppression can potentially enhance vaccine efficacy in vulnerable populations.","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":" ","pages":"1-17"},"PeriodicalIF":4.3,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142872024","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

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

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

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

Understanding innate and adaptive responses during radiation combined burn injuries. 了解辐射合并烧伤时的先天反应和适应性反应。

IF 5 4区医学

International Reviews of Immunology Pub Date : 2024-09-11 DOI: 10.1080/08830185.2024.2402023

Rishav Kumar,Ajay Kumar Sharma,Kirti,Aman Kalonia,Priyanka Shaw,M H Yashvarddhan,Arpana Vibhuti,Sandeep Kumar Shukla

{"title":"Understanding innate and adaptive responses during radiation combined burn injuries.","authors":"Rishav Kumar,Ajay Kumar Sharma,Kirti,Aman Kalonia,Priyanka Shaw,M H Yashvarddhan,Arpana Vibhuti,Sandeep Kumar Shukla","doi":"10.1080/08830185.2024.2402023","DOIUrl":"https://doi.org/10.1080/08830185.2024.2402023","url":null,"abstract":"The occurrence of incidents involving radiation-combined burn injuries (RCBI) poses a significant risk to public health. Understanding the immunological and physiological responses associated with such injuries is crucial for developing care triage to counter the mortality that occurs due to the synergistic effects of radiation and burn injuries. The core focus of this narrative review lies in unraveling the immune response against RCBI. Langerhans cells, mast cells, keratinocytes, and fibroblasts, which induce innate immunity, have been explored for their response to radiation, burns, and combined injuries. In the case of adaptive immune response, exploring behavioral changes in T regulatory (Treg) cells, T helper cells (Th1, Th2, and Th17), and immunoglobulin results in delayed healing compared to burn and radiation injury. The review also includes the function of complement system components such as neutrophils, acute phase proteins (CRP, C3, and C5), and cytokines for their role in RCBI. Combined insults resulting in a reduction in the cell population of immune cells display variation in response based on radiation doses, burn injury types, and their intrinsic radiosensitivity. The lack of approved countermeasures against RCBI poses a significant challenge. Drug repurposing might help to balance immune cell alteration, resulting in fast recovery and decreasing mortality, which gives it clinical significance for its implication on the site of such incidence. However, the exact immune response in RCBI remains insufficiently explored in pre-clinical and clinical stages, which might be due to the non-availability of in vitro models, standard animal models, or human subjects, warranting further research.","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":"35 1","pages":"1-14"},"PeriodicalIF":5.0,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142185432","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