Cytokine & Growth Factor Reviews最新文献

JAK inhibitors in immune regulation and treatment of vitiligo. JAK 抑制剂在免疫调节和白癜风治疗中的作用。

IF 9.3 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2024-11-10 DOI: 10.1016/j.cytogfr.2024.11.002

Kewei Liu, Linyi Zhou, Meihui Shi, Tianxin Cong, Xiaoyi Yang, Xiangnan Zhou, Ming Cheng, Cong Ma, Shulan Yao, Peiyao Ying, Zhenzhen Mu, Yan Wu

{"title":"JAK inhibitors in immune regulation and treatment of vitiligo.","authors":"Kewei Liu, Linyi Zhou, Meihui Shi, Tianxin Cong, Xiaoyi Yang, Xiangnan Zhou, Ming Cheng, Cong Ma, Shulan Yao, Peiyao Ying, Zhenzhen Mu, Yan Wu","doi":"10.1016/j.cytogfr.2024.11.002","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2024.11.002","url":null,"abstract":"Vitiligo, a disorder marked by hypopigmentation, significantly impacts patients' quality of life and mental health. This condition results from the reduction or dysfunction of melanocytes, which are crucial for skin and hair pigmentation. Current treatments include glucocorticoids, immunosuppressants, phototherapy, vitamin D3 analogues, and surgical interventions. Recent research has revealed that hyperactivation of Janus kinase (JAK) and its downstream signaling pathways intensifies cytotoxic T cell activity and weakens melanocytes' defense against environmental stressors. Additionally, the aberrant expression of pro-inflammatory cytokines such as Interferon-gamma (IFN-γ) and Tumor Necrosis Factor-alpha (TNF-α) plays a critical role in the pathogenesis of vitiligo by disrupting melanocyte function and promoting immune-mediated destruction. Clinical trials and basic research have demonstrated the efficacy of JAK inhibitors in modulating these cytokine pathways and promoting melanocyte repigmentation. This review provides a comprehensive analysis of JAK inhibitors, exploring their mechanisms and latest applications in regulating cytokine and skin immune responses, aiming to optimize their use in vitiligo therapy.","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681068","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

I don't know about you, but I'm feeling IL-22. 我不知道你怎么想，但我感觉到了 IL-22。

IF 9.3 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2024-11-08 DOI: 10.1016/j.cytogfr.2024.11.001

Logan S Dean, Alissa N Threatt, Kaylee Jones, Emmanuel O Oyewole, Morgan Pauly, Maëlis Wahl, Melea Barahona, Rose W Reiter, Tara M Nordgren

{"title":"I don't know about you, but I'm feeling IL-22.","authors":"Logan S Dean, Alissa N Threatt, Kaylee Jones, Emmanuel O Oyewole, Morgan Pauly, Maëlis Wahl, Melea Barahona, Rose W Reiter, Tara M Nordgren","doi":"10.1016/j.cytogfr.2024.11.001","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2024.11.001","url":null,"abstract":"Defense of the human body against damaging and pathogenic insults is a heavily regulated affair. A primary mechanism of defense at sites of insult are soluble mediators whose defensive maneuvers increase barrier integrity and promote pro-reparative and resolution processes. IL-22 is a cytokine in the IL-10 cytokine family that has garnered increased attention in recent years due to its intimate link in promoting resolution of inflammatory insults, while simultaneously being over expressed in certain fibrotic and chronic inflammatory-skewed diseases. The spatial action of IL-22 centers around the barrier sites of the body, including the skin, lungs, and gut mucosa. As such, a detailed understanding of the role of this cytokine, the producers and responders, and the diseases resulting from over- or under-expression have prominent impacts on a variety of disease outcomes. Herein we present a comprehensive review of IL-22; from historical perspectives and initial discovery, as well as more recent data that dramatically expands on the cellular sources and impact of this cytokine. We aim to showcase the duality of IL-22 and highlight addressable gaps in the field of IL-22 crosstalk and impacts at the ever-important mucosal and tissue barrier sites.","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616449","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

Glioblastoma-associated macrophages: A key target in overcoming glioblastoma therapeutic resistance. 胶质母细胞瘤相关巨噬细胞：克服胶质母细胞瘤耐药性的关键靶点

IF 9.3 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2024-10-31 DOI: 10.1016/j.cytogfr.2024.10.009

Aymane Kricha, Najat Bouchmaa, Sanae Ben Mkaddem, Abdellatif Abbaoui, Reda Ben Mrid, Rachid El Fatimy

{"title":"Glioblastoma-associated macrophages: A key target in overcoming glioblastoma therapeutic resistance.","authors":"Aymane Kricha, Najat Bouchmaa, Sanae Ben Mkaddem, Abdellatif Abbaoui, Reda Ben Mrid, Rachid El Fatimy","doi":"10.1016/j.cytogfr.2024.10.009","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2024.10.009","url":null,"abstract":"Glioblastoma multiforme (GBM) is recognized as the most aggressive and malignant form of brain cancer, characterized by a highly heterogeneous phenotype, poor prognosis, and a median survival time of less than 16 months. Recent studies have highlighted the critical role of glioblastoma-associated macrophages (GAMs) in promoting tumor progression and resistance not only to immunotherapy but also to radiotherapy and chemotherapy. GAMs actively suppress immune responses, promote angiogenesis, facilitate tumor metastasis, and induce therapy resistance, through various mechanisms such as cytokines production, signaling pathways regulation, and angiogenesis. In this context, understanding these regulatory mechanisms is essential for developing efficient therapies. Preclinical studies have investigated diverse approaches to target these cells, both as monotherapies or in combination with other treatments. While these approaches have shown promise in strengthening antitumor immune responses in animal models, their clinical success remains to be fully determined. Herein, we provide a comprehensive overview of GAMs's role in GBM therapeutic resistance and summarizes existing approaches to target GAMs in overcoming tumor resistance.","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603050","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 role of transforming growth factor β in cervical carcinogenesis. 转化生长因子β在宫颈癌变中的作用。

IF 9.3 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2024-10-22 DOI: 10.1016/j.cytogfr.2024.10.006

Kleber Paiva Trugilo, Guilherme Cesar Martelossi Cebinelli, Eliza Pizarro Castilha, Mariane Ricciardi da Silva, Fernanda Costa Brandão Berti, Karen Brajão de Oliveira

{"title":"The role of transforming growth factor β in cervical carcinogenesis.","authors":"Kleber Paiva Trugilo, Guilherme Cesar Martelossi Cebinelli, Eliza Pizarro Castilha, Mariane Ricciardi da Silva, Fernanda Costa Brandão Berti, Karen Brajão de Oliveira","doi":"10.1016/j.cytogfr.2024.10.006","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2024.10.006","url":null,"abstract":"Human papillomavirus (HPV) is involved in virtually all cases of cervical cancer. However, HPV alone is not sufficient to cause malignant development. The effects of chronic inflammation and the interaction of immune components with the microenvironment infected with the high-risk HPV type (HR) may contribute to cancer development. Transforming growth factor β (TGFB) appears to play an important role in cervical carcinogenesis. Protein and mRNA levels of this cytokine gradually increase as normal tissue develops into malignant tissue and are closely related to the severity of HPV infection. At the onset of infection, TGFB can inhibit the proliferation of infected cells and viral amplification by inhibiting cell growth and downregulating the transcriptional activity of the long control region (LCR) of HPV, thereby reducing the expression of early genes. When infected cells progress to a malignant phenotype, the response to the cell growth inhibitory effect of TGFB1 is lost and the suppression of E6 and E7 expression decreases. Subsequently, TGFB1 expression is upregulated by high levels of E6 and E7 oncoproteins, leading to an increase in TGFB1 in the tumor microenvironment, where this molecule promotes epithelial-to-mesenchymal transition (EMT), cell motility, angiogenesis, and immunosuppression. This interaction between HPV oncoproteins and TGFB1 is an important mechanism promoting the development and progression of cervical cancer.","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557381","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

Impact of chronic stress on intestinal mucosal immunity in colorectal cancer progression. 慢性压力对结直肠癌进展过程中肠粘膜免疫的影响

IF 9.3 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2024-10-22 DOI: 10.1016/j.cytogfr.2024.10.007

Shengya Yang, Ying Li, Yingru Zhang, Yan Wang

引用次数: 0

Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: Implications for heart failure and transplantation. Galectin-3 在心脏炎症和纤维化交叉点上的核心作用：对心力衰竭和移植的影响。

IF 9.3 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2024-10-20 DOI: 10.1016/j.cytogfr.2024.10.002

Ignacio M Seropian, Mohammad El-Diasty, Adham H El-Sherbini, Germán E González, Gabriel A Rabinovich

{"title":"Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: Implications for heart failure and transplantation.","authors":"Ignacio M Seropian, Mohammad El-Diasty, Adham H El-Sherbini, Germán E González, Gabriel A Rabinovich","doi":"10.1016/j.cytogfr.2024.10.002","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2024.10.002","url":null,"abstract":"Cardiac inflammation and fibrosis are central pathogenic mechanisms leading to heart failure. Transplantation is still the treatment of choice for many patients undergoing end-stage heart failure who remain symptomatic despite optimal medical therapy. In spite of considerable progress, the molecular mechanisms linking inflammation, fibrosis and heart failure remain poorly understood. Galectin-3 (GAL3), a chimera-type member of the galectin family, has emerged as a critical mediator implicated in cardiac inflammatory, vascular and fibrotic processes through modulation of different cellular compartments including monocytes and macrophages, fibroblasts, endothelial cells and vascular smooth muscle cells via glycan-dependent or independent mechanisms. GAL3-driven circuits may hierarchically amplify cytokine production and function, immune cell activation and fibrosis cascades, influencing a wide range of cardiovascular disorders. Thus, GAL3 emerges as a potential therapeutic target to counteract aberrant inflammation and fibrosis during heart failure and a potential biomarker of heart failure and clinical outcome of heart transplantation.","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557380","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

Unraveling the intricacies of neutrophil extracellular traps in inflammatory bowel disease: Pathways, biomarkers, and promising therapies. 揭开炎症性肠病中中性粒细胞胞外捕获物的神秘面纱：途径、生物标志物和有前景的疗法。

IF 9.3 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2024-10-18 DOI: 10.1016/j.cytogfr.2024.10.003

Yilin Wu, Jun Shen

{"title":"Unraveling the intricacies of neutrophil extracellular traps in inflammatory bowel disease: Pathways, biomarkers, and promising therapies.","authors":"Yilin Wu, Jun Shen","doi":"10.1016/j.cytogfr.2024.10.003","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2024.10.003","url":null,"abstract":"The development of inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease, involves various factors and is characterized by persistent inflammation of the mucosal lining. However, the role of neutrophils in this process remains controversial. Neutrophil extracellular traps (NETs), which consist of chromatin, antimicrobial proteins, and oxidative enzymes, are released by neutrophils to trap pathogens. They are also involved in various immune-mediated and vascular diseases. NETs act as a vital defense mechanisms at the gut-mucosal interface and are frequently exposed to bacterial, viral, and fungal threats. However, they can also contribute to inflammation and worsen imbalances in the gut bacteria. Recent studies have suggested that NETs have a significant impact on IBD development. Previous studies have shown increased levels of NETs in tissue and blood samples from patients with IBD, as well as in experimental colitis mouse models. Therefore, this review discusses how NETs are formed and their role in the pathophysiology of IBD. It discusses how NETs may lead to tissue damage and contribute to IBD-associated complications. Moreover, non-invasive biomarkers are needed to replace invasive procedures such as endoscopy to better evaluate the disease status. Given the crucial role of NETs in IBD progression, this review focuses on potential NET biomarkers that can help predict the evolution of IBD. Furthermore, this review identifies potential therapeutic targets for regulating NET production, which could expand the range of available treatment options for IBD.","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142496809","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

Distinct roles of MIF in the pathogenesis of ischemic heart disease. MIF 在缺血性心脏病发病机制中的不同作用。

IF 9.3 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2024-10-16 DOI: 10.1016/j.cytogfr.2024.10.005

Ling Zhao, Bang-Hao Zhao, Amanguli Ruze, Qiu-Lin Li, An-Xia Deng, Xiao-Ming Gao

{"title":"Distinct roles of MIF in the pathogenesis of ischemic heart disease.","authors":"Ling Zhao, Bang-Hao Zhao, Amanguli Ruze, Qiu-Lin Li, An-Xia Deng, Xiao-Ming Gao","doi":"10.1016/j.cytogfr.2024.10.005","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2024.10.005","url":null,"abstract":"The role of macrophage migration inhibitory factor (MIF) as a multifunctional cytokine in immunomodulation and inflammatory response is increasingly appreciated. Ischemic heart disease (IHD), the leading cause of global mortality, remains a focal point of research owing to its intricate pathophysiology. MIF has been identified as a critical player in IHD, where it exerts distinct roles. On one hand, MIF plays a protective role by enhancing energy metabolism through activation of AMPK, resisting oxidative stress, inhibiting activation of the JNK pathway, and maintaining intracellular calcium ion homeostasis. Additionally, MIF exerts protective effects through mesenchymal stem cells and exosomes. On the other hand, MIF can assume a pro-inflammatory role, which contributes to the exacerbation of IHD's development and progression. Furthermore, MIF levels significantly increase in IHD patients, and its genetic polymorphisms are positively correlated with prevalence and severity. These findings position MIF as a potential biomarker and therapeutic target in the management of IHD. This review summarizes the structure, source, signaling pathways and biological functions of MIF and focuses on its roles and clinical characteristics in IHD. The genetic variants of MIF associated with IHD is also discussed, providing more understandings of its complex interplay in the disease's pathology.","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142496807","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

NLRP1 inflammasome in neurodegenerative disorders: From pathology to therapies. 神经退行性疾病中的 NLRP1 炎症小体：从病理学到疗法

IF 9.3 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2024-10-16 DOI: 10.1016/j.cytogfr.2024.10.004

Meng-Jie Zhang, Long Yang, Zhuo-Yao Li, Long-Yun Zhou, Yong-Jun Wang, Hong-Shen Wang, Xue-Jun Cui, Min Yao

{"title":"NLRP1 inflammasome in neurodegenerative disorders: From pathology to therapies.","authors":"Meng-Jie Zhang, Long Yang, Zhuo-Yao Li, Long-Yun Zhou, Yong-Jun Wang, Hong-Shen Wang, Xue-Jun Cui, Min Yao","doi":"10.1016/j.cytogfr.2024.10.004","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2024.10.004","url":null,"abstract":"Neuroinflammation is a critical component in neurodegenerative disorders. The inflammasome, facilitates the cleavage of caspase-1, leading to the maturation and subsequent secretion of inflammatory factors interleukin (IL)-1β and IL-18. Consequently, pyroptosis mediated by gasdermin D, exacerbates neuroinflammation. Among the inflammasomes, NLRP1/3 are predominant in the central nervous system (CNS), Although NLRP1 was the earliest discovered inflammasome, the specific involvement of NLRP1 in neurodegenerative diseases remains to be fully elucidated. Recently, the discovery of an endogenous inhibitor of NLRP1, dipeptidyl peptidase 9, suggests the feasibility of producing of small-molecule drugs targeting NLRP1. This review describes the latest findings on the role of the NLRP1 inflammasome in the pathology of neurodegenerative disorders, including Alzheimer's disease, and summarises the regulatory mechanisms of NLRP1 inflammasome activation in the CNS. Furthermore, we highlight the recent progress in developing small-molecule and biological inhibitors that modulate the NLRP1 infammasome for the treatment of neurodegenerative disorders, some of which are advancing to preclinical testing. SIGNIFICANCE STATEMENT: The objective of this review is to synthesise the research on the structure, activation, and regulatory mechanisms of the NLRP1 inflammasome, along with its potential impact on both acute and chronic neurodegenerative conditions. The discovery of endogenous inhibitors, such as dipeptidyl peptidase 9 and thioredoxin, and their interaction with NLRP1 suggest the possibility of developing NLRP1-targeted small-molecule drugs for the treatment of neurodegenerative disorders. This review also discusses the use of both direct and indirect NLRP1 inhibitors as prospective therapeutic strategies for these conditions.","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142496808","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 Yin and Yang of TLR4 in COVID-19. TLR4 在 COVID-19 中的阴与阳。

IF 9.3 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2024-10-09 DOI: 10.1016/j.cytogfr.2024.10.001

Suprabhat Mukherjee, Jagadeesh Bayry

{"title":"The Yin and Yang of TLR4 in COVID-19.","authors":"Suprabhat Mukherjee, Jagadeesh Bayry","doi":"10.1016/j.cytogfr.2024.10.001","DOIUrl":"https://doi.org/10.1016/j.cytogfr.2024.10.001","url":null,"abstract":"Various pattern recognition receptors (PRRs), including toll-like receptors (TLRs), play a crucial role in recognizing invading pathogens as well as damage-associated molecular patterns (DAMPs) released in response to infection. The resulting signaling cascades initiate appropriate immune responses to eliminate these pathogens. Current evidence suggests that SARS-CoV-2-driven activation of TLR4, whether through direct recognition of the spike glycoprotein (alone or in combination with endotoxin) or by sensing various TLR4-activating DAMPs or alarmins released during viral infection, acts as a critical mediator of antiviral immunity. However, TLR4 exerts a dual role in COVID-19, demonstrating both beneficial and deleterious effects. Dysregulated TLR4 signaling is implicated in the proinflammatory consequences linked to the immunopathogenesis of COVID-19. Additionally, TLR4 polymorphisms contribute to severity of the disease. Given its significant immunoregulatory impact on COVID-19 immunopathology and host immunity, TLR4 has emerged as a key target for developing inhibitors and immunotherapeutic strategies to mitigate the adverse effects associated with SARS-CoV-2 and related infections. Furthermore, TLR4 agonists are also being explored as adjuvants to enhance immune responses to SARS-CoV-2 vaccines.","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":" ","pages":""},"PeriodicalIF":9.3,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567799","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