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Interleukin-17: A pleiotropic cytokine implicated in inflammatory, infectious, and malignant disorders.
IF 9.3 2区 医学
Cytokine & Growth Factor Reviews Pub Date : 2025-01-23 DOI: 10.1016/j.cytogfr.2025.01.002
Anushka Saran, Daisuke Nishizaki, Scott M Lippman, Shumei Kato, Razelle Kurzrock
{"title":"Interleukin-17: A pleiotropic cytokine implicated in inflammatory, infectious, and malignant disorders.","authors":"Anushka Saran, Daisuke Nishizaki, Scott M Lippman, Shumei Kato, Razelle Kurzrock","doi":"10.1016/j.cytogfr.2025.01.002","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2025.01.002","url":null,"abstract":"<p><p>IL-17A, referred to as IL-17, is the founding member of a family of pro-inflammatory cytokines, including IL-17B, IL-17C, IL-17D, IL-17E (or IL-25), and IL-17F, which act via receptors IL-17RA to IL-17RE, and elicit potent cellular responses that impact diverse diseases. IL-17's interactions with various cytokines include forming a heterodimer with IL-17F and being stimulated by IL-23's activation of Th17 cells, which can lead to inflammation and autoimmunity. IL-17 is implicated in infectious diseases and inflammatory disorders such as rheumatoid arthritis and psoriasis, promoting neutrophil recruitment and anti-bacterial immunity, but potentially exacerbating fungal and viral infections, revealing its dual role as protective and pathologic. IL-17 is also involved in various cancers, including breast, colon, cervical, prostate, and skin cancer, contributing to proliferation, immune invasion, and metastases, but also playing a protective role in certain instances. Four FDA-approved drugs-secukinumab (for ankylosing spondylitis, enthesitis-related arthritis, hidradenitis suppurativa, non-radiographic axial spondyloarthritis, plaque psoriasis, and psoriatic arthritis), ixekizumab (for ankylosing spondylitis, non-radiographic axial spondyloarthritis, plaque psoriasis, and psoriatic arthritis), brodalumab (for plaque psoriasis), and bimekizumab (for plaque psoriasis)-suppress the IL-17 pathway, with more in development, including netakimab, sonelokimab, izokibep, and CJM112. These agents and others are being studied across a spectrum of disorders. Understanding the complicated interplay between IL-17 and other immune mediators may yield new treatments for inflammatory/autoimmune conditions and malignancies.</p>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058205","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}
引用次数: 0
Molecular regulation of mitophagy signaling in tumor microenvironment and its targeting for cancer therapy.
IF 9.3 2区 医学
Cytokine & Growth Factor Reviews Pub Date : 2025-01-17 DOI: 10.1016/j.cytogfr.2025.01.004
Bishnu Prasad Behera, Soumya Ranjan Mishra, Srimanta Patra, Kewal Kumar Mahapatra, Chandra Sekhar Bhol, Debasna Pritimanjari Panigrahi, Prakash Priyadarshi Praharaj, Daniel J Klionsky, Sujit Kumar Bhutia
{"title":"Molecular regulation of mitophagy signaling in tumor microenvironment and its targeting for cancer therapy.","authors":"Bishnu Prasad Behera, Soumya Ranjan Mishra, Srimanta Patra, Kewal Kumar Mahapatra, Chandra Sekhar Bhol, Debasna Pritimanjari Panigrahi, Prakash Priyadarshi Praharaj, Daniel J Klionsky, Sujit Kumar Bhutia","doi":"10.1016/j.cytogfr.2025.01.004","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2025.01.004","url":null,"abstract":"<p><p>Aberrations emerging in mitochondrial homeostasis are restrained by mitophagy to control mitochondrial integrity, bioenergetics signaling, metabolism, oxidative stress, and apoptosis. The mitophagy-accompanied mitochondrial processes that occur in a dysregulated condition act as drivers for cancer occurrence. In addition, the enigmatic nature of mitophagy in cancer cells modulates the cellular proteome, creating challenges for therapeutic interventions. Several reports found the role of cellular signaling pathways in cancer to modulate mitophagy to mitigate stress, immune checkpoints, energy demand, and cell death. Thus, targeting mitophagy to hinder oncogenic intracellular signaling by promoting apoptosis, in hindsight, might have an edge against cancer. This review highlights the receptors and adaptors, and the involvement of many proteins in mitophagy and their role in oncogenesis. It also provides insight into using mitophagy as a potential target for therapeutic intervention in various cancer types.</p>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143064099","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}
引用次数: 0
Insights into IL-6/JAK/STAT3 signaling in the tumor microenvironment: Implications for cancer therapy.
IF 9.3 2区 医学
Cytokine & Growth Factor Reviews Pub Date : 2025-01-17 DOI: 10.1016/j.cytogfr.2025.01.003
Win Lwin Thuya, Yang Cao, Paul Chi-Lui Ho, Andrea Li-Ann Wong, Lingzhi Wang, Jianbiao Zhou, Christophe Nicot, Boon Cher Goh
{"title":"Insights into IL-6/JAK/STAT3 signaling in the tumor microenvironment: Implications for cancer therapy.","authors":"Win Lwin Thuya, Yang Cao, Paul Chi-Lui Ho, Andrea Li-Ann Wong, Lingzhi Wang, Jianbiao Zhou, Christophe Nicot, Boon Cher Goh","doi":"10.1016/j.cytogfr.2025.01.003","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2025.01.003","url":null,"abstract":"<p><p>The IL-6/JAK/STAT3 signaling pathway is a key regulator of tumor progression, immune evasion, and therapy resistance in various cancers. Frequently dysregulated in malignancies, this pathway drives cancer cell growth, survival, angiogenesis, and metastasis by altering the tumor microenvironment (TME). IL-6 activates JAK kinases and STAT3 through its receptor complex, leading to the transcription of oncogenic genes and fostering an immunosuppressive TME. This environment recruits tumor-associated macrophages (TAMs), cancer-associated fibroblasts (CAFs), and regulatory T cells (Tregs), collectively supporting immune evasion and tumor growth. IL-6/JAK/STAT3 axis also contributes to metabolic reprogramming, such as enhanced glycolysis and glutathione metabolism, helping cancer cells adapt to environmental stresses. Therapeutic targeting of this pathway has gained significant interest. Strategies include monoclonal antibodies against IL-6 or its receptor (e.g., Tocilizumab, Siltuximab), JAK inhibitors (e.g., Ruxolitinib), and STAT3-specific inhibitors (e.g., Napabucasin), which have exhibited promise in preclinical and initial clinical studies. These inhibitors can suppress tumor growth, reverse immune suppression, and enhance the efficacy of immunotherapies like immune checkpoint inhibitors. Combination therapies that integrate IL-6 pathway inhibitors with conventional treatments are particularly promising, addressing resistance mechanisms and improving patient outcomes. Advances in biomarker-driven patient selection, RNA-based therapies, and isoform-specific inhibitors pave the way for more precise interventions. This review delves into the diverse roles of IL-6/JAK/STAT3 signaling in cancer progression, therapeutic strategies targeting this pathway, and the potential for integrating these approaches into personalized medicine to enhance treatment outcomes.</p>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143074262","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}
引用次数: 0
Interleukin-6 (IL-6)-associated tumor microenvironment remodelling and cancer immunotherapy. 白细胞介素-6 (IL-6)相关的肿瘤微环境重塑和癌症免疫治疗。
IF 9.3 2区 医学
Cytokine & Growth Factor Reviews Pub Date : 2025-01-10 DOI: 10.1016/j.cytogfr.2025.01.001
Songsong Wu, Zhumin Cao, Rongying Lu, Zhenwang Zhang, Gautam Sethi, Yulai You
{"title":"Interleukin-6 (IL-6)-associated tumor microenvironment remodelling and cancer immunotherapy.","authors":"Songsong Wu, Zhumin Cao, Rongying Lu, Zhenwang Zhang, Gautam Sethi, Yulai You","doi":"10.1016/j.cytogfr.2025.01.001","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2025.01.001","url":null,"abstract":"<p><p>Interleukin-6 (IL-6) is a pro-inflammatory cytokine playing a pivotal role during inflammation and immune responses. In the recent years, the function of IL-6 in the tumor microenvironment (TME) for affecting tumorigenesis and immunotherapy response has been investigated. The genetic mutations are mainly responsible for the development of cancer, while interactions in TME are also important, involving both cancers and non-cancerous cells. IL-6 plays a significant role in these interactions, enhancing the proliferation, survival and metastasis of tumor cells through inflammatory pathways, highlighting its carcinogenic function. Multiple immune cells including macrophages, T cells, myeloid-derived suppressor cells, dendritic cells and natural killer cells can be affected by IL-6 to develop immunosuppressive TME. IL-6 can also participate in the immune evasion through increasing levels of PD-L1, compromising the efficacy of therapeutics. Notably, IL-6 exerts a double-edge sword function and it can dually increase or decrease cancer immunotherapy, providing a challenge for targeting this cytokine in cancer therapy. Highlighting the complicated function of IL-6 in TME can lead to the development of effective therapeutics for cancer immunity.</p>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143001775","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}
引用次数: 0
Mechanisms coupling the mTOR pathway to chronic obstructive pulmonary disease (COPD) pathogenesis. mTOR通路与慢性阻塞性肺疾病(COPD)发病机制的耦合
IF 9.3 2区 医学
Cytokine & Growth Factor Reviews Pub Date : 2025-01-03 DOI: 10.1016/j.cytogfr.2024.12.005
Ankita Goyal, Vishal Chopra, Kranti Garg, Siddharth Sharma
{"title":"Mechanisms coupling the mTOR pathway to chronic obstructive pulmonary disease (COPD) pathogenesis.","authors":"Ankita Goyal, Vishal Chopra, Kranti Garg, Siddharth Sharma","doi":"10.1016/j.cytogfr.2024.12.005","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2024.12.005","url":null,"abstract":"<p><p>Chronic Obstructive Pulmonary Disease (COPD) is a poorly reversible respiratory disorder distinguished by dyspnea, cough, expectoration and exacerbations due to abnormality of airways or emphysema. In this review, we consider the therapeutic potential of targeting Mammalian target of Rapamycin (mTOR) for treating COPD. The mTOR is a highly conserved serine-threonine protein kinase that integrates signals from growth factors and nutrients to control protein synthesis, lipid biogenesis and metabolism. Dysregulated mTOR pathway signaling due to genetic factors or cigarette smoking impairs autophagy, driving the buildup of abnormal cells and damaged proteins, resulting in inflammation and oxidative stress. Persistent mTOR activation also contributes to pulmonary vascular cell proliferation, facilitating the development of pulmonary resistance in COPD. Rapamycin, an inhibitor of mTOR, prevents the buildup of senescent cells in the lungs of COPD patients and inhibits the release of lung tissue-damaging proteases. mTOR also impacts the corticosteroid sensitivity in COPD patients by regulating the levels of histone deacetylases. The emerging role of gut-lung axis dysbiosis in the progression of COPD and its influence on mTOR further highlights the relevance of the mTOR pathway in COPD pathophysiology.</p>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970020","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}
引用次数: 0
Nuclear translocation of RON receptor tyrosine kinase. New mechanistic and functional insights. RON受体酪氨酸激酶的核易位。新的机制和功能见解。
IF 9.3 2区 医学
Cytokine & Growth Factor Reviews Pub Date : 2025-01-02 DOI: 10.1016/j.cytogfr.2024.12.004
Yi-Lin Chen, Chien-An Chu, Jiu-Yao Wang, Wan-Li Chen, Yi-Wen Wang, Chung-Liang Ho, Chung-Ta Lee, Nan-Haw Chow
{"title":"Nuclear translocation of RON receptor tyrosine kinase. New mechanistic and functional insights.","authors":"Yi-Lin Chen, Chien-An Chu, Jiu-Yao Wang, Wan-Li Chen, Yi-Wen Wang, Chung-Liang Ho, Chung-Ta Lee, Nan-Haw Chow","doi":"10.1016/j.cytogfr.2024.12.004","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2024.12.004","url":null,"abstract":"<p><p>Receptor tyrosine kinases (RTKs) are membrane sensors that monitor alterations in the extracellular milieu and translate this information into appropriate cellular responses. Epidermal growth factor receptor (EGFR) is the most well-known model in which gene expression is upregulated by mitogenic signals through the activation of multiple signaling cascades or by nuclear translocation of the full-length EGFR protein. RON (Receptuer d'Origine Nantatise, also known as macrophage stimulating 1 receptor, MST1R) has recently gained attention as a therapeutic target for human cancer. This review summarizes the recent understanding of the unusual nuclear translocation of uncleaved RON receptor proteins in response to cellular stresses, such as serum starvation, hormonal deprivation, hypoxia, and genotoxicity. This nonligand mechanism, achieved by RON per se or by interaction with EGFR, may directly activate the transcriptional machinery necessary for cancer cells to survive. In vitro experiments have demonstrated the importance of tyrosine kinase of RON in binding to and activating the c-JUN promoter, HIF-1α, DNA helicase 2, DNA-dependent protein kinase catalytic subunit, and other stress-responsive networks. Nuclear RON-activated nonhomologous end joining repair confers chemoresistance to drugs that induce double-strand breaks (DSBs) in cancer cells. Tyrosine kinase inhibitors or monoclonal antibodies targeting RON kinase may therefore be useful treatments for patients with RON-overexpressing tumors. DSB-inducing anticancer drugs are not recommended for these cancer patients. Moreover, multi-RTK inhibition is a more rational strategy for patients with RON- and RTK-coexpressing human cancer.</p>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142964013","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}
引用次数: 0
The immunopathogenesis of a cytokine storm: The key mechanisms underlying severe COVID-19.
IF 9.3 2区 医学
Cytokine & Growth Factor Reviews Pub Date : 2025-01-02 DOI: 10.1016/j.cytogfr.2024.12.003
Luka Hiti, Tijana Markovič, Mitja Lainscak, Jerneja Farkaš Lainščak, Emil Pal, Irena Mlinarič-Raščan
{"title":"The immunopathogenesis of a cytokine storm: The key mechanisms underlying severe COVID-19.","authors":"Luka Hiti, Tijana Markovič, Mitja Lainscak, Jerneja Farkaš Lainščak, Emil Pal, Irena Mlinarič-Raščan","doi":"10.1016/j.cytogfr.2024.12.003","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2024.12.003","url":null,"abstract":"<p><p>A cytokine storm is marked by excessive pro-inflammatory cytokine release, and has emerged as a key factor in severe COVID-19 cases - making it a critical therapeutic target. However, its pathophysiology was poorly understood, which hindered effective treatment. SARS-CoV-2 initially disrupts angiotensin signalling, promoting inflammation through ACE-2 downregulation. Some patients' immune systems then fail to shift from innate to adaptive immunity, suppressing interferon responses and leading to excessive pyroptosis and neutrophil activation. This amplifies tissue damage and inflammation, creating a pro-inflammatory loop. The result is the disruption of Th1/Th2 and Th17/Treg balances, lymphocyte exhaustion, and extensive blood clotting. Cytokine storm treatments include glucocorticoids to suppress the immune system, monoclonal antibodies to neutralize specific cytokines, and JAK inhibitors to block cytokine receptor signalling. However, the most effective treatment options for mitigating SARS-CoV-2 infection remain vaccines as a preventive measure and antiviral drugs for the early stages of infection. This article synthesizes insights into immune dysregulation in COVID-19, offering a framework to better understand cytokine storms and to improve monitoring, biomarker discovery, and treatment strategies for COVID-19 and other conditions involving cytokine storms.</p>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143064253","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}
引用次数: 0
Granulocyte macrophage colony stimulating factor in virus-host interactions and its implication for immunotherapy. 粒细胞巨噬细胞集落刺激因子在病毒-宿主相互作用及其对免疫治疗的意义。
IF 9.3 2区 医学
Cytokine & Growth Factor Reviews Pub Date : 2024-12-26 DOI: 10.1016/j.cytogfr.2024.12.002
Nasry Zane Bouzeineddine, Alecco Philippi, Katrina Gee, Sam Basta
{"title":"Granulocyte macrophage colony stimulating factor in virus-host interactions and its implication for immunotherapy.","authors":"Nasry Zane Bouzeineddine, Alecco Philippi, Katrina Gee, Sam Basta","doi":"10.1016/j.cytogfr.2024.12.002","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2024.12.002","url":null,"abstract":"<p><p>Viruses have evolved to strategically exploit cellular signaling pathways to evade host immune defenses. GM-CSF signaling plays a pivotal role in regulating inflammation, activating myeloid cells, and enhancing the immune response to infections. Due to its central role in the immune system, viruses may target this pathway to further establish infection. This review focuses on key studies elucidating virus interactions with GM-CSF signaling proteins and summarizes findings on the impact of viral infections on GM-CSF production. Additionally, therapeutic strategies centered around GM-CSF are investigated, such as the potential benefits of administering GM-CSF versus inhibiting GM-CSF signaling to mitigate viral-induced aberrant inflammation. Understanding these virus-host interactions provides valuable insights that help further our understanding to develop future therapeutic approaches in modulating the immune response during viral infections.</p>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926931","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}
引用次数: 0
LC3B: A microtubule-associated protein influences disease progression and prognosis. LC3B:一种微管相关蛋白影响疾病进展和预后。
IF 9.3 2区 医学
Cytokine & Growth Factor Reviews Pub Date : 2024-12-12 DOI: 10.1016/j.cytogfr.2024.11.006
Yan Chen, Hong Yi, Shan Liao, Junyu He, Yanhong Zhou, Yan Lei
{"title":"LC3B: A microtubule-associated protein influences disease progression and prognosis.","authors":"Yan Chen, Hong Yi, Shan Liao, Junyu He, Yanhong Zhou, Yan Lei","doi":"10.1016/j.cytogfr.2024.11.006","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2024.11.006","url":null,"abstract":"<p><p>Microtubule-associated protein 1 light chain 3B (MAP1LC3B, also known as LC3B) is a mammalian homolog of the autophagy-related protein 8 (ATG8) family. It plays a crucial role in cellular autophagy and is involved in several vital biological processes, including apoptosis and differentiation. Additionally, LC3B regulates immune responses. Due to its close association with malignant tumors and neurodegenerative diseases, and its potential as a prognostic indicator and therapeutic target, LC3B has become a significant research focus. This article aims to provide a comprehensive and systematic understanding of LC3B's role and mechanisms in autophagy, its impact on apoptosis and the underlying mechanisms, its regulation of cellular differentiation and transdifferentiation, its modulation of immune and inflammatory responses, the influence of upstream regulatory factors on LC3B's function, and its relevance to disease diagnosis, treatment, and prognosis. The goal is to establish a solid foundation for understanding LC3B's role in cellular processes and its regulatory mechanisms.</p>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863556","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}
引用次数: 0
Cytokine signalling in formation of neutrophil extracellular traps: Implications for health and diseases. 中性粒细胞胞外陷阱形成中的细胞因子信号传导:对健康和疾病的影响。
IF 9.3 2区 医学
Cytokine & Growth Factor Reviews Pub Date : 2024-12-09 DOI: 10.1016/j.cytogfr.2024.12.001
Haritha Manoj, Sarah Michael Gomes, Pooja Yedehalli Thimmappa, Prabhakara R Nagareddy, Colin Jamora, Manjunath B Joshi
{"title":"Cytokine signalling in formation of neutrophil extracellular traps: Implications for health and diseases.","authors":"Haritha Manoj, Sarah Michael Gomes, Pooja Yedehalli Thimmappa, Prabhakara R Nagareddy, Colin Jamora, Manjunath B Joshi","doi":"10.1016/j.cytogfr.2024.12.001","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2024.12.001","url":null,"abstract":"<p><p>Neutrophils, as essential component of the innate immune response, form a crucial part in the defence mechanisms through the release of extracellular traps (NETs). These web-like structures, composed of chromatin and antimicrobial proteins, are essential for the entrapment and inactivation of pathogens. However, either constitutive formation or inefficient clearance of NETs leads to adverse effects such as fibrosis, thrombosis, delayed wound healing and tissue damage in multiple diseases associated with sterile inflammation. This dichotomy casts NETs as both protective agents and harmful factors in several diseases such as autoimmune diseases, metabolic syndromes, systemic infections, and malignancies. Besides microbes and their products, variety of stimulants including pro-inflammatory cytokines induce NETs. The complex interactions and cross talk among the pro-inflammatory cytokines including IL-8, IL-6, GM-CSF, TNF-α, IFNs, and IL-1β activate neutrophils to form NETs and also contributes to a vicious circle of inflammatory cascade, leading to increased inflammation, oxidative stress, and thrombotic events. Emerging evidence indicates that the dysregulated cytokine milieus in diseases, such as diabetes mellitus, obesity, atherosclerosis, stroke, rheumatoid arthritis, and systemic lupus erythematosus, potentiate NETs release, thereby promoting disease development. Thus, neutrophils represent both critical effectors and potential therapeutic targets, underscoring their importance in the context of cytokine-mediated therapies for a spectrum of diseases. In the present review, we describe various cytokines and associated signalling pathways activating NETs formation in different human pathologies. Further, the review identifies potential strategies to pharmacologically modulate cytokine pathways to reduce NETs.</p>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142834415","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}
引用次数: 0
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