Pub Date : 2024-02-01DOI: 10.1016/j.cytogfr.2023.08.004
Xiaoqian Zhai , Yiyun Lin , Lingling Zhu , Yuqing Wang , Jiabi Zhang , Jiewei Liu , Lu Li , Xiaojie Lu
Ferroptosis is a type of cell death characterized by iron-dependent phospholipid peroxidation and reactive oxygen species overproduction. Ferroptosis induces immunogenic cell death and elicits anti-tumor immune responses, playing an important role in cancer immunotherapy. Ferroptosis suppression in cancer cells impairs its immunotherapeutic efficacy. To overcome this issue, ferroptosis inducers (FINs) have been combined with other cancer therapies to create an anti-tumor immune microenvironment. However, the ferroptosis-based crosstalk between immune and tumor cells is complex because oxidative products released by ferroptotic tumor cells impair the functions of anti-tumor immune cells, resulting in immunotherapeutic resistance. In the present article, we have reviewed ferroptosis in tumor and immune cells and summarized the crosstalk between ferroptotic tumor cells and the immune microenvironment. Based on the existing literature, we have further discussed future perspectives on opportunities for combining ferroptosis-targeted therapies with cancer immunotherapies.
{"title":"Ferroptosis in cancer immunity and immunotherapy: Multifaceted interplay and clinical implications","authors":"Xiaoqian Zhai , Yiyun Lin , Lingling Zhu , Yuqing Wang , Jiabi Zhang , Jiewei Liu , Lu Li , Xiaojie Lu","doi":"10.1016/j.cytogfr.2023.08.004","DOIUrl":"10.1016/j.cytogfr.2023.08.004","url":null,"abstract":"<div><p>Ferroptosis is a type of cell death characterized by iron-dependent phospholipid peroxidation and reactive oxygen species overproduction. Ferroptosis induces immunogenic cell death and elicits anti-tumor immune responses, playing an important role in cancer immunotherapy. Ferroptosis suppression in cancer cells impairs its immunotherapeutic efficacy. To overcome this issue, ferroptosis inducers (FINs) have been combined with other cancer therapies to create an anti-tumor immune microenvironment. However, the ferroptosis-based crosstalk between immune and tumor cells is complex because oxidative products released by ferroptotic tumor cells impair the functions of anti-tumor immune cells, resulting in immunotherapeutic resistance. In the present article, we have reviewed ferroptosis in tumor and immune cells and summarized the crosstalk between ferroptotic tumor cells and the immune microenvironment. Based on the existing literature, we have further discussed future perspectives on opportunities for combining ferroptosis-targeted therapies with cancer immunotherapies.</p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":null,"pages":null},"PeriodicalIF":13.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1359610123000515/pdfft?md5=c015942f30fa49f8abdee35054c3a07c&pid=1-s2.0-S1359610123000515-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10194164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-01DOI: 10.1016/j.cytogfr.2023.10.002
Eslam E Saad , Rachel Michel , Mostafa A. Borahay
Uterine fibroids (UF), also called uterine leiomyoma, is one of the most prevalent uterine tumors. UF represents a serious women's health global problem with a significant physical, emotional, and socioeconomic impact. Risk factors for UF include racial disparities, age, race, hormonal factors, obesity, and lifestyle (diet, physical activity, and stress. There are several biological contributors to UF pathogenesis such as cellular proliferation, angiogenesis, and extracellular matrix (ECM) accumulation. This review addresses tumor immune microenvironment as a novel mediator of ECM deposition. Polarization of immune microenvironment towards the immunosuppressive phenotype has been associated with ECM deposition. Immunosuppressive cells include M2 macrophage, myeloid-derived suppressor cells (MDSCs), and Th17 cells, and their secretomes include interleukin 4 (IL-4), IL-10, IL-13, IL-17, IL-22, arginase 1, and transforming growth factor-beta (TGF-β1). The change in the immune microenvironment not only increase tumor growth but also aids in collagen synthesis and ECM disposition, which is one of the main hallmarks of UF pathogenesis. This review invites further investigations on the change in the UF immune microenvironment as well as a novel targeting approach instead of the traditional UF hormonal and supportive treatment.
{"title":"Immunosuppressive tumor microenvironment and uterine fibroids: Role in collagen synthesis","authors":"Eslam E Saad , Rachel Michel , Mostafa A. Borahay","doi":"10.1016/j.cytogfr.2023.10.002","DOIUrl":"10.1016/j.cytogfr.2023.10.002","url":null,"abstract":"<div><p>Uterine fibroids (UF), also called uterine leiomyoma, is one of the most prevalent uterine tumors. UF represents a serious women's health global problem with a significant physical, emotional, and socioeconomic impact. Risk factors for UF include racial disparities, age, race, hormonal factors, obesity, and lifestyle (diet, physical activity, and stress. There are several biological contributors to UF pathogenesis such as cellular proliferation, angiogenesis, and extracellular matrix (ECM) accumulation. This review addresses tumor immune microenvironment as a novel mediator of ECM deposition. Polarization of immune microenvironment towards the immunosuppressive phenotype has been associated with ECM deposition. Immunosuppressive cells include M2 macrophage, myeloid-derived suppressor cells (MDSCs), and Th17 cells, and their secretomes include interleukin 4 (IL-4), IL-10, IL-13, IL-17, IL-22, arginase 1, and transforming growth factor-beta (TGF-β1). The change in the immune microenvironment not only increase tumor growth but also aids in collagen synthesis and ECM disposition, which is one of the main hallmarks of UF pathogenesis. This review invites further investigations on the change in the UF immune microenvironment as well as a novel targeting approach instead of the traditional UF hormonal and supportive treatment.</p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":null,"pages":null},"PeriodicalIF":13.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41233201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-01DOI: 10.1016/j.cytogfr.2023.11.002
Yang Zhou , Ann Richmond , Chi Yan
CD40 is a member of the tumor necrosis factor (TNF) receptor superfamily of receptors expressed on a variety of cell types. The CD40–CD40L interaction gives rise to many immune events, including the licensing of dendritic cells to activate CD8+ effector T cells, as well as the facilitation of B cell activation, proliferation, and differentiation. In malignant cells, the expression of CD40 varies among cancer types, mediating cellular proliferation, apoptosis, survival and the secretion of cytokines and chemokines. Agonistic human anti-CD40 antibodies are emerging as an option for cancer treatment, and early-phase clinical trials explored its monotherapy or combination with radiotherapy, chemotherapy, immune checkpoint blockade, and other immunomodulatory approaches. In this review, we present the current understanding of the mechanism of action for CD40, along with results from the clinical development of agonistic human CD40 antibodies in cancer treatment (selicrelumab, CDX-1140, APX005M, mitazalimab, 2141-V11, SEA-CD40, LVGN7409, and bispecific antibodies). This review also examines the safety profile of CD40 agonists in both preclinical and clinical settings, highlighting optimized dosage levels, potential adverse effects, and strategies to mitigate them.
{"title":"Harnessing the potential of CD40 agonism in cancer therapy","authors":"Yang Zhou , Ann Richmond , Chi Yan","doi":"10.1016/j.cytogfr.2023.11.002","DOIUrl":"10.1016/j.cytogfr.2023.11.002","url":null,"abstract":"<div><p>CD40 is a member of the tumor necrosis factor (TNF) receptor superfamily of receptors expressed on a variety of cell types. The CD40–CD40L interaction gives rise to many immune events, including the licensing of dendritic cells to activate CD8<sup>+</sup> effector T cells, as well as the facilitation of B cell activation, proliferation, and differentiation. In malignant cells, the expression of CD40 varies among cancer types, mediating cellular proliferation, apoptosis, survival and the secretion of cytokines and chemokines. Agonistic human anti-CD40 antibodies are emerging as an option for cancer treatment, and early-phase clinical trials explored its monotherapy or combination with radiotherapy, chemotherapy, immune checkpoint blockade, and other immunomodulatory approaches. In this review, we present the current understanding of the mechanism of action for CD40, along with results from the clinical development of agonistic human CD40 antibodies in cancer treatment (selicrelumab, CDX-1140, APX005M, mitazalimab, 2141-V11, SEA-CD40, LVGN7409, and bispecific antibodies). This review also examines the safety profile of CD40 agonists in both preclinical and clinical settings, highlighting optimized dosage levels, potential adverse effects, and strategies to mitigate them.</p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":null,"pages":null},"PeriodicalIF":13.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1359610123000795/pdfft?md5=e2336dcb3765155f17297d0ef320fa9c&pid=1-s2.0-S1359610123000795-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138526205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-01DOI: 10.1016/j.cytogfr.2023.11.003
Lihui Xuan , Chenjun Bai , Zhao Ju , Jinhua Luo , Hua Guan , Ping-Kun Zhou , Ruixue Huang
In contemporary oncology, radiation therapy and immunotherapy stand as critical treatments, each with distinct mechanisms and outcomes. Radiation therapy, a key player in cancer management, targets cancer cells by damaging their DNA with ionizing radiation. Its effectiveness is heightened when used alongside other treatments like surgery and chemotherapy. Employing varied radiation types like X-rays, gamma rays, and proton beams, this approach aims to minimize damage to healthy tissue. However, it is not without risks, including potential damage to surrounding normal cells and side effects ranging from skin inflammation to serious long-term complications. Conversely, immunotherapy marks a revolutionary step in cancer treatment, leveraging the body’s immune system to target and destroy cancer cells. It manipulates the immune system’s specificity and memory, offering a versatile approach either alone or in combination with other treatments. Immunotherapy is known for its targeted action, long-lasting responses, and fewer side effects compared to traditional therapies. The interaction between radiation therapy and immunotherapy is intricate, with potential for both synergistic and antagonistic effects. Their combined use can be more effective than either treatment alone, but careful consideration of timing and sequence is essential. This review explores the impact of various radiation therapy regimens on immunotherapy, focusing on changes in the immune microenvironment, immune protein expression, and epigenetic factors, emphasizing the need for personalized treatment strategies and ongoing research to enhance the efficacy of these combined therapies in cancer care.
{"title":"Radiation-targeted immunotherapy: A new perspective in cancer radiotherapy","authors":"Lihui Xuan , Chenjun Bai , Zhao Ju , Jinhua Luo , Hua Guan , Ping-Kun Zhou , Ruixue Huang","doi":"10.1016/j.cytogfr.2023.11.003","DOIUrl":"10.1016/j.cytogfr.2023.11.003","url":null,"abstract":"<div><p>In contemporary oncology, radiation therapy and immunotherapy stand as critical treatments, each with distinct mechanisms and outcomes. Radiation therapy, a key player in cancer management, targets cancer cells by damaging their DNA with ionizing radiation. Its effectiveness is heightened when used alongside other treatments like surgery and chemotherapy. Employing varied radiation types like X-rays, gamma rays, and proton beams, this approach aims to minimize damage to healthy tissue. However, it is not without risks, including potential damage to surrounding normal cells and side effects ranging from skin inflammation to serious long-term complications. Conversely, immunotherapy marks a revolutionary step in cancer treatment, leveraging the body’s immune system to target and destroy cancer cells. It manipulates the immune system’s specificity and memory, offering a versatile approach either alone or in combination with other treatments. Immunotherapy is known for its targeted action, long-lasting responses, and fewer side effects compared to traditional therapies. The interaction between radiation therapy and immunotherapy is intricate, with potential for both synergistic and antagonistic effects. Their combined use can be more effective than either treatment alone, but careful consideration of timing and sequence is essential. This review explores the impact of various radiation therapy regimens on immunotherapy, focusing on changes in the immune microenvironment, immune protein expression, and epigenetic factors, emphasizing the need for personalized treatment strategies and ongoing research to enhance the efficacy of these combined therapies in cancer care.</p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":null,"pages":null},"PeriodicalIF":13.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138526219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This concise review navigates the intricate realm of Interleukin-6 (IL-6), an important member of the cytokine family. Beginning with an introduction to cytokines, this narrative review unfolds with the historical journey of IL-6, illuminating its evolving significance. A crucial section unravels the three distinct signaling modes employed by IL-6, providing a foundational understanding of its versatile interactions within cellular landscapes. Moving deeper, the review meticulously dissects IL-6's signaling mechanisms, unraveling the complexities of its pleiotropic effects in both physiological responses and pathological conditions. A significant focus is dedicated to the essential role IL-6 plays in inflammatory diseases, offering insights into its associations and implications for various health conditions. The review also takes a therapeutic turn by exploring the emergence of anti-IL-6 monoclonal inhibitors, marking a profound stride in treatment modalities. Diving into the molecular realm, the review explores small molecules as agents for IL-6 inhibition, providing a nuanced perspective on diverse intervention strategies. As the review embarks on the final chapters, it contemplates future aspects, offering glimpses into potential research trajectories and the evolving landscape of IL-6-related studies.
{"title":"Navigating IL-6: From molecular mechanisms to therapeutic breakthroughs","authors":"Akey Krishna Swaroop , Preeya Negi , Ayushi Kar , Esakkimuthukumar Mariappan , Jawahar Natarajan , Krishnan Namboori P.K. , Jubie Selvaraj","doi":"10.1016/j.cytogfr.2023.12.007","DOIUrl":"10.1016/j.cytogfr.2023.12.007","url":null,"abstract":"<div><p><span>This concise review navigates the intricate realm of Interleukin-6 (IL-6), an important member of the cytokine family. Beginning with an introduction to cytokines, this narrative review unfolds with the historical journey of IL-6, illuminating its evolving significance. A crucial section unravels the three distinct signaling modes employed by IL-6, providing a foundational understanding of its versatile interactions within cellular landscapes. Moving deeper, the review meticulously dissects IL-6's signaling mechanisms, unraveling the complexities of its pleiotropic effects<span> in both physiological responses and pathological conditions. A significant focus is dedicated to the essential role IL-6 plays in </span></span>inflammatory diseases<span><span>, offering insights into its associations and implications for various health conditions. The review also takes a therapeutic turn by exploring the emergence of anti-IL-6 monoclonal inhibitors, marking a profound stride in treatment modalities. Diving into the molecular realm, the review explores </span>small molecules as agents for IL-6 inhibition, providing a nuanced perspective on diverse intervention strategies. As the review embarks on the final chapters, it contemplates future aspects, offering glimpses into potential research trajectories and the evolving landscape of IL-6-related studies.</span></p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":null,"pages":null},"PeriodicalIF":13.0,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139078556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-31DOI: 10.1016/j.cytogfr.2023.12.006
Zixuan Zhou , Linru Shi , Binghai Chen , Hui Qian
The imbalance between proliferation and death of kidney resident cells is a crucial factor in the development of acute or chronic renal dysfunction. Acute kidney injury (AKI) is often associated with the rapid loss of tubular epithelial cells (TECs). Sustained injury leads to the loss of glomerular endothelial cells (GECs) and podocytes, which is a key mechanism in the pathogenesis of glomerular diseases. This irreversible damage resulting from progressive cell loss eventually leads to deterioration of renal function characterized by glomerular compensatory hypertrophy, tubular degeneration, and renal fibrosis. Regulated cell death (RCD), which involves a cascade of gene expression events with tight structures, plays a certain role in regulating kidney health by determining the fate of kidney resident cells. Under pathological conditions, cells in the nephron have been demonstrated to constitutively release extracellular vesicles (EVs) which act as messengers that specifically interact with recipient cells to regulate their cell death process. For therapeutic intervention, exogenous EVs have exhibited great potential for the prevention and treatment of kidney disease by modulating RCD, with enhanced effects through engineering modification. Based on the functional role of EVs, this review comprehensively explores the regulation of RCD by EVs in AKI and chronic kidney disease (CKD), with emphasis on pathogenesis and therapeutic intervention.
肾脏驻留细胞增殖与死亡之间的失衡是导致急性或慢性肾功能障碍的关键因素。急性肾损伤(AKI)通常与肾小管上皮细胞(TECs)的快速丧失有关。持续的损伤会导致肾小球内皮细胞(GECs)和荚膜细胞的丧失,这是肾小球疾病发病的关键机制。细胞逐渐丧失造成的这种不可逆损伤最终会导致肾功能恶化,表现为肾小球代偿性肥大、肾小管变性和肾脏纤维化。调节性细胞死亡(RCD)涉及一连串具有严密结构的基因表达事件,通过决定肾脏常驻细胞的命运,在调节肾脏健康方面发挥着一定的作用。在病理条件下,肾小球中的细胞已被证实会持续释放细胞外囊泡,这些囊泡作为信使与受体细胞发生特异性相互作用,从而调节其细胞死亡过程。在治疗干预方面,外源性EVs通过调节RCD在预防和治疗肾脏疾病方面表现出巨大的潜力,并通过工程改造增强效果。基于 EVs 的功能作用,本综述全面探讨了 EVs 在 AKI 和慢性肾脏病(CKD)中对 RCD 的调控,重点是发病机制和治疗干预。
{"title":"Regulation of regulated cell death by extracellular vesicles in acute kidney injury and chronic kidney disease","authors":"Zixuan Zhou , Linru Shi , Binghai Chen , Hui Qian","doi":"10.1016/j.cytogfr.2023.12.006","DOIUrl":"10.1016/j.cytogfr.2023.12.006","url":null,"abstract":"<div><p><span>The imbalance between proliferation and death of kidney resident cells is a crucial factor in the development of acute or chronic renal dysfunction. Acute kidney injury<span><span> (AKI) is often associated with the rapid loss of tubular epithelial cells (TECs). Sustained injury leads to the loss of glomerular endothelial cells (GECs) and </span>podocytes<span>, which is a key mechanism in the pathogenesis of glomerular diseases. This irreversible damage resulting from progressive cell loss eventually leads to deterioration of </span></span></span>renal function<span><span><span><span><span> characterized by glomerular compensatory hypertrophy, tubular degeneration, and renal fibrosis. Regulated cell death (RCD), which involves a cascade of gene expression events with tight structures, plays a certain role in regulating kidney health by determining the fate of kidney resident cells. Under pathological conditions, cells in the </span>nephron have been demonstrated to constitutively release extracellular vesicles (EVs) which act as messengers that specifically interact with recipient cells to regulate their cell death process. For therapeutic intervention, exogenous EVs have exhibited great potential for the prevention and </span>treatment of </span>kidney disease by modulating RCD, with enhanced effects through engineering modification. Based on the functional role of EVs, this review comprehensively explores the regulation of RCD by EVs in AKI and </span>chronic kidney disease (CKD), with emphasis on pathogenesis and therapeutic intervention.</span></p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":null,"pages":null},"PeriodicalIF":13.0,"publicationDate":"2023-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139066615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-30DOI: 10.1016/j.cytogfr.2023.12.005
Jinling Xu , Yanzhuo Song , Sheng Ding , Weizhe Duan , Guangda Xiang , Zhongjing Wang
Myeloid-derived growth factor (MYDGF) is a paracrine protein produced by bone marrow-derived monocytes and macrophages. Current research shows that it has protective effects on the cardiovascular system, such as repairing heart tissue after myocardial infarction, enhancing cardiomyocyte proliferation, improving cardiac regeneration after myocardial injury, regulating proliferation and survival of endothelial cells, reducing endothelial cell damage, resisting pressure overload-induced heart failure, as well as protecting against atherosclerosis. Furthermore, regarding the metabolic diseases, MYDGF has effects of improving type 2 diabetes mellitus, relieving non-alcoholic fatty liver disease, alleviating glomerular diseases, and resisting osteoporosis. Herein, we will discuss the biology of MYDGF and its effects on cardiovascular and metabolic diseases.
{"title":"Myeloid-derived growth factor and its effects on cardiovascular and metabolic diseases","authors":"Jinling Xu , Yanzhuo Song , Sheng Ding , Weizhe Duan , Guangda Xiang , Zhongjing Wang","doi":"10.1016/j.cytogfr.2023.12.005","DOIUrl":"10.1016/j.cytogfr.2023.12.005","url":null,"abstract":"<div><p><span>Myeloid-derived growth factor (MYDGF) is a paracrine protein produced by bone marrow-derived monocytes<span><span><span> and macrophages. Current research shows that it has protective effects on the cardiovascular system, such as repairing heart tissue after myocardial infarction, enhancing cardiomyocyte proliferation, improving cardiac regeneration after </span>myocardial injury, regulating proliferation and survival of </span>endothelial cells, reducing endothelial cell damage, resisting pressure overload-induced heart failure, as well as protecting against </span></span>atherosclerosis<span>. Furthermore, regarding the metabolic diseases<span>, MYDGF has effects of improving type 2 diabetes mellitus, relieving non-alcoholic fatty liver disease, alleviating glomerular diseases<span>, and resisting osteoporosis. Herein, we will discuss the biology of MYDGF and its effects on cardiovascular and metabolic diseases.</span></span></span></p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":null,"pages":null},"PeriodicalIF":13.0,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139072244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-29DOI: 10.1016/j.cytogfr.2023.12.004
Soumyalekshmi Nair , Melissa Razo-Azamar , Nanthini Jayabalan , Louise Torp Dalgaard , Berenice Palacios-González , Anne Sørensen , Ulla Kampmann , Aase Handberg , Flavio Carrion , Carlos Salomon
Cell-to-cell communication mediated by Extracellular Vesicles (EVs) is a novel and emerging area of research, especially during pregnancy, in which placenta derived EVs can facilitate the feto-maternal communication. EVs comprise a heterogeneous group of vesicle sub-populations with diverse physical and biochemical characteristics and originate by specific biogenesis mechanisms. EVs transfer molecular cargo (including proteins, nucleic acids, and lipids) between cells and are critical mediators of cell communication. There is growing interest among researchers to explore into the molecular cargo of EVs and their functions in a physiological and pathological context. For example, inflammatory mediators such as cytokines are shown to be released in EVs and EVs derived from immune cells play key roles in mediating the immune response as well as immunoregulatory pathways. Pregnancy complications such as gestational diabetes mellitus, preeclampsia, intrauterine growth restriction and preterm birth are associated with altered levels of circulating EVs, with differential EV cargo and bioactivity in target cells. This implicates the intriguing roles of EVs in reprogramming the maternal physiology during pregnancy. Moreover, the capacity of EVs to carry bioactive molecules makes them a promising tool for biomarker development and targeted therapies in pregnancy complications. This review summarizes the physiological and pathological roles played by EVs in pregnancy and pregnancy-related disorders and describes the potential of EVs to be translated into clinical applications in the diagnosis and treatment of pregnancy complications.
{"title":"Advances in extracellular vesicles as mediators of cell-to-cell communication in pregnancy","authors":"Soumyalekshmi Nair , Melissa Razo-Azamar , Nanthini Jayabalan , Louise Torp Dalgaard , Berenice Palacios-González , Anne Sørensen , Ulla Kampmann , Aase Handberg , Flavio Carrion , Carlos Salomon","doi":"10.1016/j.cytogfr.2023.12.004","DOIUrl":"10.1016/j.cytogfr.2023.12.004","url":null,"abstract":"<div><p><span><span>Cell-to-cell communication mediated by Extracellular Vesicles (EVs) is a novel and emerging area of research, especially during pregnancy, in which placenta derived EVs can facilitate the feto-maternal communication. EVs comprise a heterogeneous group of vesicle sub-populations with diverse physical and biochemical characteristics and originate by specific biogenesis mechanisms. EVs transfer molecular cargo (including proteins, </span>nucleic acids<span>, and lipids) between cells and are critical mediators of cell communication. There is growing interest among researchers to explore into the molecular cargo of EVs and their functions in a physiological and pathological context. For example, inflammatory mediators such as cytokines are shown to be released in EVs and EVs derived from </span></span>immune cells<span><span><span><span> play key roles in mediating the immune response as well as immunoregulatory pathways. Pregnancy complications such as gestational diabetes mellitus, </span>preeclampsia, </span>intrauterine growth restriction<span> and preterm birth are associated with altered levels of circulating EVs, with differential EV cargo and </span></span>bioactivity<span><span> in target cells. This implicates the intriguing roles of EVs in reprogramming the maternal physiology during pregnancy. Moreover, the capacity of EVs to carry bioactive molecules makes them a promising tool for biomarker development and targeted therapies in pregnancy complications. This review summarizes the physiological and pathological roles played by EVs in pregnancy and pregnancy-related disorders and describes the potential of EVs to be translated into clinical applications in the diagnosis and </span>treatment<span> of pregnancy complications.</span></span></span></p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":null,"pages":null},"PeriodicalIF":13.0,"publicationDate":"2023-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139071855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-14DOI: 10.1016/j.cytogfr.2023.12.001
Peng-yi He , Meng-yao Wu , Li-yu Zheng , Yu Duan , Qi Fan , Xiao-mei Zhu , Yong-ming Yao
Interleukin (IL)− 33, a nuclear factor and pleiotropic cytokine of the IL-1 family, is gaining attention owing to its important role in chronic inflammatory and autoimmune diseases. This review extends our knowledge of the effects exerted by IL-33 on target cells by binding to its specific receptor serum stimulation-2 (ST2). Depending on the tissue context, IL-33 performs multiple functions encompassing host defence, immune response, initiation and amplification of inflammation, tissue repair, and homeostasis. The levels and activity of IL-33 in the body are controlled by complex IL-33-targeting regulatory pathways. The unique temporal and spatial expression patterns of IL-33 are associated with host homeostasis and the development of immune and inflammatory disorders. Therefore, understanding the origin, function, and processes of IL-33 under various conditions is crucial. This review summarises the regulatory mechanisms underlying the IL-33/ST2 signalling axis and its potential role and clinical significance in immune and inflammatory diseases, and discusses the current complex and conflicting findings related to IL-33 in host responses.
{"title":"Interleukin-33/serum stimulation-2 pathway: Regulatory mechanisms and emerging implications in immune and inflammatory diseases","authors":"Peng-yi He , Meng-yao Wu , Li-yu Zheng , Yu Duan , Qi Fan , Xiao-mei Zhu , Yong-ming Yao","doi":"10.1016/j.cytogfr.2023.12.001","DOIUrl":"10.1016/j.cytogfr.2023.12.001","url":null,"abstract":"<div><p>Interleukin (IL)− 33, a nuclear factor and pleiotropic cytokine of the IL-1 family, is gaining attention owing to its important role in chronic inflammatory and autoimmune diseases. This review extends our knowledge of the effects exerted by IL-33 on target cells by binding to its specific receptor serum stimulation-2 (ST2). Depending on the tissue context, IL-33 performs multiple functions encompassing host defence, immune response, initiation and amplification of inflammation, tissue repair, and homeostasis. The levels and activity of IL-33 in the body are controlled by complex IL-33-targeting regulatory pathways. The unique temporal and spatial expression patterns of IL-33 are associated with host homeostasis and the development of immune and inflammatory disorders. Therefore, understanding the origin, function, and processes of IL-33 under various conditions is crucial. This review summarises the regulatory mechanisms underlying the IL-33/ST2 signalling axis and its potential role and clinical significance in immune and inflammatory diseases, and discusses the current complex and conflicting findings related to IL-33 in host responses.</p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":null,"pages":null},"PeriodicalIF":13.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1359610123000898/pdfft?md5=27d6c8274f19944ce85d64c036b93ffb&pid=1-s2.0-S1359610123000898-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138682413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-09DOI: 10.1016/j.cytogfr.2023.11.005
Thilini H. Senevirathne , Demi Wekking , Joseph W.R. Swain , Cinzia Solinas , Pushpamali De Silva
The vigorous spread of SARS-CoV-2 resulted in the rapid infection of millions of people worldwide and devastation of not only public healthcare, but also social, educational, and economic infrastructures. The evolution of SARS-CoV-2 over time is due to the mutations that occurred in the genome during each replication. These mutated forms of SARS-CoV-2, otherwise known as variants, were categorized as variants of interest (VOI) or variants of concern (VOC) based on the increased risk of transmissibility, disease severity, immune escape, decreased effectiveness of current social measures, and available vaccines and therapeutics. The swift development of COVID-19 vaccines has been a great success for biomedical research, and billions of vaccine doses, including boosters, have been administered worldwide. BNT162b2 vaccine (Pfizer–BioNTech), mRNA-1273 (Moderna), ChAdOx1 nCoV-19 (AstraZeneca), and Janssen (Johnson & Johnson) are the four major COVID-19 vaccines that received early regulatory authorization based on their efficacy. However, some SARS-CoV-2 variants resulted in higher resistance to available vaccines or treatments. It has been four years since the first reported infection of SARS-CoV-2, yet the Omicron variant and its subvariants are still infecting people worldwide. Despite this, COVID-19 vaccines are still expected to be effective at preventing severe disease, hospitalization, and death from COVID. In this review, we provide a comprehensive overview of the COVID-19 pandemic focused on evolution of VOC and vaccination strategies against them.
{"title":"COVID-19: From emerging variants to vaccination","authors":"Thilini H. Senevirathne , Demi Wekking , Joseph W.R. Swain , Cinzia Solinas , Pushpamali De Silva","doi":"10.1016/j.cytogfr.2023.11.005","DOIUrl":"10.1016/j.cytogfr.2023.11.005","url":null,"abstract":"<div><p>The vigorous spread of SARS-CoV-2 resulted in the rapid infection of millions of people worldwide and devastation of not only public healthcare, but also social, educational, and economic infrastructures. The evolution of SARS-CoV-2 over time is due to the mutations that occurred in the genome during each replication. These mutated forms of SARS-CoV-2, otherwise known as variants, were categorized as variants of interest (VOI) or variants of concern (VOC) based on the increased risk of transmissibility, disease severity, immune escape, decreased effectiveness of current social measures, and available vaccines and therapeutics. The swift development of COVID-19 vaccines has been a great success for biomedical research, and billions of vaccine doses, including boosters, have been administered worldwide. BNT162b2 vaccine (Pfizer–BioNTech), mRNA-1273 (Moderna), ChAdOx1 nCoV-19 (AstraZeneca), and Janssen (Johnson & Johnson) are the four major COVID-19 vaccines that received early regulatory authorization based on their efficacy. However, some SARS-CoV-2 variants resulted in higher resistance to available vaccines or treatments. It has been four years since the first reported infection of SARS-CoV-2, yet the Omicron variant and its subvariants are still infecting people worldwide. Despite this, COVID-19 vaccines are still expected to be effective at preventing severe disease, hospitalization, and death from COVID. In this review, we provide a comprehensive overview of the COVID-19 pandemic focused on evolution of VOC and vaccination strategies against them.</p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":null,"pages":null},"PeriodicalIF":13.0,"publicationDate":"2023-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138561332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}