International Reviews of Immunology最新文献

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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
{"title":"The NLRP3 inflammasome: Mechanisms of activation, regulation, and role in diseases.","authors":"Mina Dadkhah, Mohammadreza Sharifi","doi":"10.1080/08830185.2024.2415688","DOIUrl":"https://doi.org/10.1080/08830185.2024.2415688","url":null,"abstract":"<p><p>Because of numerous stress signals, intracellular protein complexes are called inflammasomes. They function as catalysts for the proteolytic transformation of pro-interleukin into the active form of interleukin. Inflammasomes can promote a type of cell death process known as pyroptosis. The NLRP3 inflammasome, comprised of the NLRP3 protein, procaspase-1, and ASC, tightly regulates inflammation. The NLRP3 inflammasome is activated by a variety of stimuli, and several molecular and cellular events, such as ion influx, mitochondrial dysfunction, reactive oxygen species production, and lysosomal damage have been shown to trigger its activation. Inflammation plays a major role in almost all types of human diseases. The NLRP3 inflammasome has been the most widely studied and plays an important pathogenic role in various inflammatory pathologies. This review briefly presents the basic features of NLRP3 inflammasome and their mechanisms of activation and regulation. In addition, recent studies report the role of NLRP3 inflammasome in several diseases have been summarized.</p>","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":" ","pages":"1-14"},"PeriodicalIF":4.3,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142465489","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
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
{"title":"Transforming growth factor-β in tumor microenvironment: Understanding its impact on monocytes and macrophages for its targeting.","authors":"Tetiana Hourani, Amit Sharma, Rodney B Luwor, Adrian A Achuthan","doi":"10.1080/08830185.2024.2411998","DOIUrl":"https://doi.org/10.1080/08830185.2024.2411998","url":null,"abstract":"<p><p>TGF-β is a pivotal cytokine that orchestrates various aspects of cancer progression, including tumor growth, metastasis, and immune evasion. In this review, we present a comprehensive overview of the multifaceted role of transforming growth factor β (TGF-β) in cancer biology, focusing on its intricate interactions with monocytes and macrophages within the tumor microenvironment (TME). We specifically discuss how TGF-β modulates monocyte and macrophage activities, leading to immunosuppression and tumor progression. We conclude with the current translational and clinical efforts targeting TGF-β, recognizing the promising role of this strategy in immunooncology.</p>","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":" ","pages":"1-16"},"PeriodicalIF":4.3,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390519","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
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":"<p><p>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 <i>in vitro</i> model of asthma.FUNDC1 down-regulation promoted IL-4, IL-5, IL-10 and IL-13 activity levels <i>in vitro</i> 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.</p>","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":"<p><p>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<sup>+</sup> 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.</p>","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
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
Immunological processes of enhancers and suppressors of long non-coding RNAs associated with brain tumors and inflammation. 与脑肿瘤和炎症相关的长链非编码rna的增强子和抑制子的免疫过程。
IF 5 4区 医学
International Reviews of Immunology Pub Date : 2024-05-01 Epub Date: 2023-11-17 DOI: 10.1080/08830185.2023.2280581
Hossein Tahmasebi Dehkordi, Fatemeh Khaledi, Sorayya Ghasemi
{"title":"Immunological processes of enhancers and suppressors of long non-coding RNAs associated with brain tumors and inflammation.","authors":"Hossein Tahmasebi Dehkordi, Fatemeh Khaledi, Sorayya Ghasemi","doi":"10.1080/08830185.2023.2280581","DOIUrl":"10.1080/08830185.2023.2280581","url":null,"abstract":"<p><p>Immunological processes, such as inflammation, can both cause tumor suppression and cancer progression. Moreover, deregulated levels of long non-coding RNA (lncRNA) expression in the brain may cause inflammation and lead to the growth of tumors. Like other biological processes, the immune system's role in cancer is complicated, varies, and can help or hurt the cancer's maintenance. According to research, inflammation and brain cancer are correlated <i>via</i> several signaling pathways. A variety of lncRNAs have recently been revealed to influence cancer by modulating inflammatory pathways. As a result, lncRNAs have the potential to influence carcinogenesis, tumor formation, or tumor suppression <i>via</i> an increase or decrease in inflammation functions. Although the study and targeting of lncRNAs have made great progress in the treatment of cancer, there are definitely limitations and challenges. Using new technologies like nanocarriers and cell-penetrating peptides (CPPs) to target treatments without hurting healthy body tissues has shown to be very effective. In this review article, we have collected significantly related lncRNAs and their inhibitory or stimulating roles in inflammation and brain cancer for the first time. However, there are limitations, such as side effects and damage to normal tissues. With the advancement of new targeting technologies, these lncRNAs may be candidates for the specific targeting therapy of brain cancers by limiting inflammation or stimulating the immune system against them in the future.</p>","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":" ","pages":"178-196"},"PeriodicalIF":5.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136397399","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
Low-dose IL-2 therapy in autoimmune diseases: An update review. 低剂量IL-2治疗自身免疫性疾病:最新综述。
IF 5 4区 医学
International Reviews of Immunology Pub Date : 2024-05-01 Epub Date: 2023-10-26 DOI: 10.1080/08830185.2023.2274574
Ruizhi Zhang, Yuyang Zhao, Xiangming Chen, Zhuoqing Zhuang, Xiaomin Li, Erxia Shen
{"title":"Low-dose IL-2 therapy in autoimmune diseases: An update review.","authors":"Ruizhi Zhang, Yuyang Zhao, Xiangming Chen, Zhuoqing Zhuang, Xiaomin Li, Erxia Shen","doi":"10.1080/08830185.2023.2274574","DOIUrl":"10.1080/08830185.2023.2274574","url":null,"abstract":"<p><p>Regulatory T (Treg) cells are essential for maintaining self-immune tolerance. Reduced numbers or functions of Treg cells have been involved in the pathogenesis of various autoimmune diseases and allograft rejection. Therefore, the approaches that increase the pool or suppressive function of Treg cells <i>in vivo</i> could be a general strategy to treat different autoimmune diseases and allograft rejection. Interleukin-2 (IL-2) is essential for the development, survival, maintenance, and function of Treg cells, constitutively expressing the high-affinity receptor of IL-2 and sensitive response to IL-2 <i>in vivo</i>. And low-dose IL-2 therapy <i>in vivo</i> could restore the imbalance between autoimmune response and self-tolerance toward self-tolerance <i>via</i> promoting Treg cell expansion and inhibiting follicular helper T (Tfh) and IL-17-producing helper T (Th17) cell differentiation. Currently, low-dose IL-2 treatment is receiving extensive attention in autoimmune disease and transplantation treatment. In this review, we summarize the biology of IL-2/IL-2 receptor, the mechanisms of low-dose IL-2 therapy in autoimmune diseases, the application in the progress of different autoimmune diseases, including Systemic Lupus Erythematosus (SLE), Type 1 Diabetes (T1D), Rheumatoid Arthritis (RA), Autoimmune Hepatitis (AIH), Alopecia Areata (AA), Immune Thrombocytopenia (ITP) and Chronic graft-versus-host-disease (GVHD). We also discuss the future directions to optimize low-dose IL-2 treatments.</p>","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":" ","pages":"113-137"},"PeriodicalIF":5.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50161599","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
STATs signaling pathways in dendritic cells: As potential therapeutic targets? 树突状细胞中的STATs信号通路:作为潜在的治疗靶点?
IF 5 4区 医学
International Reviews of Immunology Pub Date : 2024-05-01 Epub Date: 2023-10-27 DOI: 10.1080/08830185.2023.2274576
Sepideh Sohrabi, Javad Masoumi, Bahar Naseri, Farid Ghorbaninezhad, Shiva Alipour, Tohid Kazemi, Javad Ahmadian Heris, Leili Aghebati Maleki, Pedram Basirjafar, Raziyeh Zandvakili, Mohammad Amin Doustvandi, Behzad Baradaran
{"title":"STATs signaling pathways in dendritic cells: As potential therapeutic targets?","authors":"Sepideh Sohrabi, Javad Masoumi, Bahar Naseri, Farid Ghorbaninezhad, Shiva Alipour, Tohid Kazemi, Javad Ahmadian Heris, Leili Aghebati Maleki, Pedram Basirjafar, Raziyeh Zandvakili, Mohammad Amin Doustvandi, Behzad Baradaran","doi":"10.1080/08830185.2023.2274576","DOIUrl":"10.1080/08830185.2023.2274576","url":null,"abstract":"<p><p>Dendritic cells (DCs) are professional antigen-presenting cells (APCs), including heterogenous populations with phenotypic and functional diversity that coordinate bridging innate and adaptive immunity. Signal transducer and activator of transcriptions (STAT) factors as key proteins in cytokine signaling were shown to play distinct roles in the maturation and antigen presentation of DCs and play a pivotal role in modulating immune responses mediated by DCs such as differentiation of T cells to T helper (Th) 1, Th2 or regulatory T (Treg) cells. This review sheds light on the importance of STAT transcription factors' signaling pathways in different subtypes of DCs and highlights their targeting potential usages for improving DC-based immunotherapies for patients who suffer from cancer or diverse autoimmune conditions according to the type of the STAT transcription factor and its specific activating or inhibitory agent.</p>","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":" ","pages":"138-159"},"PeriodicalIF":5.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54229078","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
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