Cytokine & Growth Factor Reviews最新文献

{"title":"Deciphering the roles of the HMGB family in cancer: Insights from subcellular localization dynamics","authors":"Junqing Jiang ,&nbsp;Mengyu Sun ,&nbsp;Yufei Wang ,&nbsp;Wenjie Huang ,&nbsp;Limin Xia","doi":"10.1016/j.cytogfr.2024.07.004","DOIUrl":"10.1016/j.cytogfr.2024.07.004","url":null,"abstract":"<div><p>The high-mobility group box (HMGB) family consists of four DNA-binding proteins that regulate chromatin structure and function. In addition to their intracellular functions, recent studies have revealed their involvement as extracellular damage-associated molecular patterns (DAMPs), contributing to immune responses and tumor development. The HMGB family promotes tumorigenesis by modulating multiple processes including proliferation, metabolic reprogramming, metastasis, immune evasion, and drug resistance. Due to the predominant focus on HMGB1 in the literature, little is known about the remaining members of this family. This review summarizes the structural, distributional, as well as functional similarities and distinctions among members of the HMGB family, followed by a comprehensive exploration of their roles in tumor development. We emphasize the distributional and functional hierarchy of the HMGB family at both the organizational and subcellular levels, with a focus on their relationship with the tumor immune microenvironment (TIME), aiming to prospect potential strategies for anticancer therapy.</p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"78 ","pages":"Pages 85-104"},"PeriodicalIF":9.3,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1359610124000479/pdfft?md5=a65551c1464936b1783919a088e2ab79&pid=1-s2.0-S1359610124000479-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141632956","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}

{"title":"Targeting cytokines in psoriatic arthritis","authors":"Laura Neurath ,&nbsp;Michael Sticherling ,&nbsp;Georg Schett ,&nbsp;Filippo Fagni","doi":"10.1016/j.cytogfr.2024.06.001","DOIUrl":"10.1016/j.cytogfr.2024.06.001","url":null,"abstract":"<div><p>Psoriatic arthritis (PsA) is part of the psoriatic disease spectrum and is characterized by a chronic inflammatory process that affects entheses, tendons and joints. Cytokines produced by immune and non-immune cells play a central role in the pathogenesis of PsA by orchestrating key aspects of the inflammatory response. Pro-inflammatory cytokines such as TNF, IL-23 and IL-17 have been shown to regulate the initiation and progression of PsA, ultimately leading to the destruction of the architecture of the local tissues such as soft tissue, cartilage and bone. The important role of cytokines in PsA has been underscored by the clinical success of antibodies that neutralize their function. In addition to biologic agents targeting individual pro-inflammatory cytokines, signaling inhibitors that block multiple cytokines simultaneously such as JAK inhibitors have been approved for PsA therapy. In this review, we will focus on our current understanding of the role of cytokines in the disease process of PsA and discuss potential new treatment options based on modulation of cytokine function.</p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"78 ","pages":"Pages 1-13"},"PeriodicalIF":9.3,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S135961012400042X/pdfft?md5=adc6bfb36f1f954a114753ffae983ed3&pid=1-s2.0-S135961012400042X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141787484","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}

{"title":"Inflammatory mechanisms of preterm labor and emerging anti-inflammatory interventions","authors":"Tiffany Habelrih ,&nbsp;Thalyssa-Lyn Augustin ,&nbsp;Félix Mauffette-Whyte ,&nbsp;Béatrice Ferri ,&nbsp;Kevin Sawaya ,&nbsp;France Côté ,&nbsp;Mathilde Gallant ,&nbsp;David M. Olson ,&nbsp;Sylvain Chemtob","doi":"10.1016/j.cytogfr.2024.07.007","DOIUrl":"10.1016/j.cytogfr.2024.07.007","url":null,"abstract":"<div><p>Preterm birth is a major public health concern, requiring a deeper understanding of its underlying inflammatory mechanisms and to develop effective therapeutic strategies. This review explores the complex interaction between inflammation and preterm labor, highlighting the pivotal role of the dysregulation of inflammation in triggering premature delivery. The immunological environment of pregnancy, characterized by a fragile balance of immune tolerance and resistance, is disrupted in preterm labor, leading to a pathological inflammatory response. Feto-maternal infections, among other pro-inflammatory stimuli, trigger the activation of toll-like receptors and the production of pro-inflammatory mediators, promoting uterine contractility and cervical ripening. Emerging anti-inflammatory therapeutics offer promising approaches for the prevention of preterm birth by targeting key inflammatory pathways. From TLR-4 antagonists to chemokine and interleukin receptor antagonists, these interventions aim to modulate the inflammatory environment and prevent adverse pregnancy outcomes. In conclusion, a comprehensive understanding of the inflammatory mechanisms leading to preterm labor is crucial for the development of targeted interventions in hope of reducing the incidence of preterm birth and improving neonatal health outcomes.</p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"78 ","pages":"Pages 50-63"},"PeriodicalIF":9.3,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1359610124000509/pdfft?md5=2403b9f286170e6cf880483df8910c29&pid=1-s2.0-S1359610124000509-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141757730","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}

{"title":"The journey of STING: Guiding immune signaling through membrane trafficking","authors":"Jingyi He ,&nbsp;Leiliang Zhang","doi":"10.1016/j.cytogfr.2024.07.003","DOIUrl":"10.1016/j.cytogfr.2024.07.003","url":null,"abstract":"<div><p><span>Stimulator of Interferon Genes (STING) serves as a pivotal mediator in the innate immune </span>signaling pathway<span><span>, transducing signals from various DNA receptors and playing a crucial role in natural immune processes. During cellular quiescence<span>, STING protein resides in the endoplasmic reticulum<span><span> (ER), and its activation typically occurs through the cGAS-STING signaling pathway. Upon activation, STING protein is transported to the </span>Golgi apparatus<span><span>, thereby initiating downstream signaling cascades. Vesicular transport serves as the primary mechanism for STING protein trafficking between the ER and Golgi apparatus, with COPII mediating anterograde transport from the ER to Golgi apparatus, while </span>COPI<span><span> is responsible for retrograde transport. Numerous factors influence these transport processes, thereby exerting either promoting or inhibitory effects on STING protein expression. Upon reaching the Golgi apparatus, to prevent over-activation, STING protein is transported to post-Golgi compartments for degradation. In addition to the conventional lysosomal degradation pathway, </span>ESCRT has also been identified as one of the degradation pathways for STING protein. This review summarizes the recent findings on the membrane trafficking pathways of STING, highlighting their contributions to the regulation of </span></span></span></span></span>cytokine production<span>, the activation of immune cells, and the coordination of immune signaling pathways.</span></span></p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"78 ","pages":"Pages 25-36"},"PeriodicalIF":9.3,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141632958","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}

{"title":"Unveiling cytokine charge disparity as a potential mechanism for immune regulation","authors":"Jennifer M. Messina ,&nbsp;Minghao Luo ,&nbsp;Md Shanewaz Hossan ,&nbsp;Hadil A. Gadelrab ,&nbsp;Xiguang Yang ,&nbsp;Anna John ,&nbsp;Joel R. Wilmore ,&nbsp;Juntao Luo","doi":"10.1016/j.cytogfr.2023.12.002","DOIUrl":"10.1016/j.cytogfr.2023.12.002","url":null,"abstract":"<div><p>Cytokines are small signaling proteins that regulate the immune responses to infection and tissue damage. Surface charges of cytokines determine their in vivo fate in immune regulation, e.g., half-life and distribution. The overall negative charges in the extracellular microenvironment and the acidosis during inflammation and infection may differentially impact cytokines with different surface charges for fine-tuned immune regulation via controlling tissue residential properties. However, the trend and role of cytokine surface charges has yet to be elucidated in the literature. Interestingly, we have observed that most pro-inflammatory cytokines have a negative charge, while most anti-inflammatory cytokines and chemokines have a positive charge. In this review, we extensively examined the surface charges of all cytokines and chemokines, summarized the pharmacokinetics and tissue adhesion of major cytokines, and analyzed the link of surface charge with cytokine biodistribution, activation, and function in immune regulation. Additionally, we identified that the general trend of charge disparity between pro- and anti-inflammatory cytokines represents a unique opportunity to develop precise immune modulation approaches, which can be applied to many inflammation-associated diseases including solid tumors, chronic wounds, infection, and sepsis.</p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"77 ","pages":"Pages 1-14"},"PeriodicalIF":9.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139053367","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}

{"title":"From orphan to oncogene: The role of GPR35 in cancer and immune modulation","authors":"Simran Takkar ,&nbsp;Gunjan Sharma ,&nbsp;Jyoti B. Kaushal ,&nbsp;K.M. Abdullah ,&nbsp;Surinder K. Batra ,&nbsp;Jawed A. Siddiqui","doi":"10.1016/j.cytogfr.2024.03.004","DOIUrl":"10.1016/j.cytogfr.2024.03.004","url":null,"abstract":"<div><p>G protein-coupled receptors (GPCRs) are well-studied and the most traceable cell surface receptors for drug discovery. One of the intriguing members of this family is G protein-coupled receptors 35 (GPR35), which belongs to the class A rhodopsin-like family of GPCRs identified over two decades ago. GPR35 presents interesting features such as ubiquitous expression and distinct isoforms. Moreover, functional and genome-wide association studies on its widespread expression have linked GPR35 with pathophysiological disease progression. Various pieces of evidence have been accumulated regarding the independent or endogenous ligand-dependent role of GPR35 in cancer progression and metastasis. In the current scenario, the relationship of this versatile receptor and its putative endogenous ligands for the activation of oncogenic signal transduction pathways at the cellular level is an active area of research. These intriguing features offered by GPR35 make it an oncological target, justifying its uniqueness at the physiological and pathophysiological levels concerning other GPCRs. For pharmacologically targeting receptor-induced signaling, few potential competitive antagonists have been discovered that offer high selectivity at a human level. In addition to its fascinating features, targeting GPR35 at rodent and human orthologue levels is distinct, thus contributing to the sub-species selectivity. Strategies to modulate these issues will help us understand and truly target GPR35 at the therapeutic level. In this article, we have provided prospects on each topic mentioned above and suggestions to overcome the challenges. This review discusses the molecular mechanism and signal transduction pathways activated by endogenous ligands or spontaneous auto-activation of GPR35 that contributes towards disease progression. Furthermore, we have highlighted the GPR35 structure, ubiquitous expression, its role in immunomodulation, and at the pathophysiological level, especially in cancer, indicating its status as a versatile receptor. Subsequently, we discussed the various proposed ligands and their mechanism of interaction with GPR35. Additionally, we have summarized the GPR35 antagonist that provides insights into the opportunities for therapeutically targeting this receptor.</p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"77 ","pages":"Pages 56-66"},"PeriodicalIF":9.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140184000","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}

{"title":"Macrophage migration inhibitor factor (MIF): Potential role in cognitive impairment disorders","authors":"Lian Zeng ,&nbsp;Pengchao Hu ,&nbsp;Yu Zhang ,&nbsp;Mingyue Li ,&nbsp;Yilin Zhao ,&nbsp;Shiyong Li ,&nbsp;Ailin Luo","doi":"10.1016/j.cytogfr.2024.03.003","DOIUrl":"10.1016/j.cytogfr.2024.03.003","url":null,"abstract":"<div><p>Macrophage migration inhibitory factor (MIF) is a cytokine in the immune system, participated in both innate and adaptive immune responses. Except from immune cells, MIF is also secreted by a variety of non-immune cells, including hematopoietic cells, endothelial cells (ECs), and neurons. MIF plays a crucial role in various diseases, such as sepsis, rheumatoid arthritis, acute kidney injury, and neurodegenerative diseases. The role of MIF in the neuropathogenesis of cognitive impairment disorders is emphasized, as it recruits multiple inflammatory mediators, leading to activating microglia or astrocyte-derived neuroinflammation. Furthermore, it contributes to the cell death of neurons and ECs with the binding of apoptosis-inducing factor (AIF) through parthanatos-associated apoptosis-inducing factor nuclease (PAAN) / MIF pathway. This review comprehensively delves into the relationship between MIF and the neuropathogenesis of cognitive impairment disorders, providing a series of emerging MIF-targeted pharmaceuticals as potential treatments for cognitive impairment disorders.</p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"77 ","pages":"Pages 67-75"},"PeriodicalIF":9.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140271342","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}

{"title":"Z-DNA binding protein 1 orchestrates innate immunity and inflammatory cell death","authors":"Qixiang Song ,&nbsp;Yuhang Fan ,&nbsp;Huali Zhang ,&nbsp;Nian Wang","doi":"10.1016/j.cytogfr.2024.03.005","DOIUrl":"10.1016/j.cytogfr.2024.03.005","url":null,"abstract":"<div><p>Innate immunity is not only the first line of host defense against microbial infections but is also crucial for the host responses against a variety of noxious stimuli. Z-DNA binding protein 1 (ZBP1) is a cytosolic nucleic acid sensor that can induce inflammatory cell death in both immune and nonimmune cells upon sensing of incursive virus-derived Z-form nucleic acids and self-nucleic acids via its Zα domain. Mechanistically, aberrantly expressed or activated ZBP1 induced by pathogens or noxious stimuli enables recruitment of TANK binding kinase 1 (TBK1), interferon regulatory factor 3 (IRF3), receptor-interacting serine/threonine-protein kinase 1 (RIPK1) and RIPK3 to drive type I interferon (IFN-I) responses and activation of nuclear factor kappa B (NF-κB) signaling. Meanwhile, ZBP1 promotes the assembly of ZBP1- and absent in melanoma 2 (AIM2)-PANoptosome, which ultimately triggers PANoptosis through caspase 3-mediated apoptosis, mixed lineage kinase domain like pseudokinase (MLKL)-mediated necroptosis, and gasdermin D (GSDMD)-mediated pyroptosis. In response to damaged mitochondrial DNA, ZBP1 can interact with cyclic GMP-AMP synthase to augment IFN-I responses but inhibits toll like receptor 9-mediated inflammatory responses. This review summarizes the structure and expression pattern of ZBP1, discusses its roles in human diseases through immune-dependent (<em>e.g.</em>, the production of IFN-I and pro-inflammatory cytokines) and -independent (<em>e.g.</em>, the activation of cell death) functions, and highlights the attractive prospect of manipulating ZBP1 as a promising therapeutic target in diseases.</p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"77 ","pages":"Pages 15-29"},"PeriodicalIF":9.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140317987","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}

{"title":"Corrigendum to “Immune evasion of neutralizing antibodies by SARS-CoV-2 Omicron” [Cytokine Growth Factor Rev. 70 (2023) 13–25]","authors":"Lidong Wang ,&nbsp;Michelle Møhlenberg ,&nbsp;Pengfei Wang ,&nbsp;Hao Zhou","doi":"10.1016/j.cytogfr.2024.03.006","DOIUrl":"10.1016/j.cytogfr.2024.03.006","url":null,"abstract":"","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"77 ","pages":"Page 117"},"PeriodicalIF":9.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1359610124000339/pdfft?md5=c30cfec166409537e65972caab277d2c&pid=1-s2.0-S1359610124000339-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140768261","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}

{"title":"Exogenous drug-induced mouse models of atopic dermatitis","authors":"Rou Zheng ,&nbsp;Yan Ren ,&nbsp;Xinyue Liu ,&nbsp;Canxia He ,&nbsp;Hua Liu ,&nbsp;Yixuan Wang ,&nbsp;Jianing Li ,&nbsp;Shuya Xia ,&nbsp;Zhifang Liu ,&nbsp;Yizhao Ma ,&nbsp;Dianchen Wang ,&nbsp;Suling Xu ,&nbsp;Geng Wang ,&nbsp;Na Li","doi":"10.1016/j.cytogfr.2024.01.003","DOIUrl":"10.1016/j.cytogfr.2024.01.003","url":null,"abstract":"<div><p>Atopic dermatitis (AD) is an inflammatory skin disease characterized by intense pruritus. AD is harmful to both children and adults, but its pathogenic mechanism has yet to be fully elucidated. The development of mouse models for AD has greatly contributed to its study and treatment. Among these models, the exogenous drug-induced mouse model has shown promising results and significant advantages. Until now, a large amount of AD-related research has utilized exogenous drug-induced mouse models, leading to notable advancements in research. This indicates the crucial significance of applying such models in AD research. These models exhibit diverse characteristics and are highly complex. They involve the use of various strains of mice, diverse types of inducers, and different modeling effects. However, there is currently a lack of comprehensive comparative studies on exogenous drug-induced AD mouse models, which hinders researchers' ability to choose among these models. This paper provides a comprehensive review of the features and mechanisms associated with various exogenous drug-induced mouse models, including the important role of each cytokine in AD development. It aims to assist researchers in quickly understanding models and selecting the most suitable one for further investigation.</p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"77 ","pages":"Pages 104-116"},"PeriodicalIF":9.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139463027","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}