As the most prevalent companion animal, cats are threatened by numerous infectious diseases and carry zoonotic pathogens such as Toxoplasma gondii and Bartonella henselae, which are the primary causes of human toxoplasmosis and cat-scratch disease. Vaccines play a crucial role in preventing and controlling the spread of diseases in both humans and animals. Currently, there are only three core vaccines available to prevent feline panleukopenia, feline herpesvirus, and feline calicivirus infections, with few vaccines available for other significant feline infectious and zoonotic diseases. Feline herpesvirus, a major component of the core vaccine, offers several advantages and a stable genetic manipulation platform, making it an ideal model for vaccine vector development to prevent and control feline infectious diseases. This paper reviews the technologies involved in the research and development of the feline herpesvirus vaccine vector, including homologous recombination, CRISPR/Cas9, and bacterial artificial chromosomes. It also examines the design and effectiveness of expressing antigens of other pathogens using the feline herpesvirus as a vaccine vector. Additionally, the paper analyzes existing technical bottlenecks and challenges, providing an outlook on its application prospects. The aim of this review is to provide a scientific basis for the research and development of feline herpesvirus as a vaccine vector and to offer new ideas for the prevention and control of significant feline infectious and zoonotic diseases.
{"title":"Advancements, challenges, and future perspectives in developing feline herpesvirus 1 as a vaccine vector","authors":"Xinru Luo, Ruiying Liang, Lin Liang, Aoxing Tang, Shaohua Hou, Jiabo Ding, Zibin Li, Xinming Tang","doi":"10.3389/fimmu.2024.1445387","DOIUrl":"https://doi.org/10.3389/fimmu.2024.1445387","url":null,"abstract":"As the most prevalent companion animal, cats are threatened by numerous infectious diseases and carry zoonotic pathogens such as <jats:italic>Toxoplasma gondii</jats:italic> and <jats:italic>Bartonella henselae</jats:italic>, which are the primary causes of human toxoplasmosis and cat-scratch disease. Vaccines play a crucial role in preventing and controlling the spread of diseases in both humans and animals. Currently, there are only three core vaccines available to prevent feline panleukopenia, feline herpesvirus, and feline calicivirus infections, with few vaccines available for other significant feline infectious and zoonotic diseases. Feline herpesvirus, a major component of the core vaccine, offers several advantages and a stable genetic manipulation platform, making it an ideal model for vaccine vector development to prevent and control feline infectious diseases. This paper reviews the technologies involved in the research and development of the feline herpesvirus vaccine vector, including homologous recombination, CRISPR/Cas9, and bacterial artificial chromosomes. It also examines the design and effectiveness of expressing antigens of other pathogens using the feline herpesvirus as a vaccine vector. Additionally, the paper analyzes existing technical bottlenecks and challenges, providing an outlook on its application prospects. The aim of this review is to provide a scientific basis for the research and development of feline herpesvirus as a vaccine vector and to offer new ideas for the prevention and control of significant feline infectious and zoonotic diseases.","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142222475","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 : 2024-09-12DOI: 10.3389/fimmu.2024.1444222
Qian Yang, Bixia Duan, Jian Yue, Donglin Zhang, Xueping Chen, Mengjia Shi, Jie Kan, Ruochan Li, Hongda Li, Lin Gan
ObjectiveThe involvement of immune cells in colorectal cancer (CRC) and their interplay with metabolic disorders are yet to be fully elucidated. This study examines how peripheral immune cells, inferred genetically, affect CRC and investigates the intermediary roles of metabolites.MethodsWe employed a two-sample bidirectional Mendelian randomization (MR) approach to assess the causal influence of immune cells on CRC. Additionally, a two-step MR strategy was utilized to pinpoint potential metabolites that mediate this effect. Our analysis incorporated data from genome-wide association studies (GWAS), involving 731 immune cell types, 1,400 metabolites, and CRC outcomes. The primary method of analysis was randomized inverse variance weighting (IVW), supported by MR-Egger, weighted median, simple mode, and weighted mode analyses. Sensitivity checks were conducted using Cochran’s Q test, MR-PRESSO test, MR-Egger regression intercept, and leave-one-out analysis.ResultsThe study identified 23 immune cell types and 17 metabolites that are causally linked to CRC. Our mediation analysis highlighted that nine metabolites act as intermediaries in the relationship between nine specific immune cells and CRC risk. Notably, The ratios of Adenosine 5’-monophosphate (AMP) to aspartate and Retinol (Vitamin A) to linoleoyl-arachidonoyl-glycerol (18:2 to 20:4) were found to concurrently mediate the promoting effects of Myeloid DC %DC and BAFF-R on B cells in colorectal cancer (CRC). Moreover, iminodiacetate (IDA) was found to mediate the protective effect of CD14+ CD16- monocytes on CRC, contributing 11.8% to this mediation. In contrast, IDA was also seen to decrease the protective effect of IgD+ CD38br %B cells on CRC risk, with a mediation effect proportion of -10.4%.ConclusionThis study delineates a complex network involving immune cells, metabolites, and CRC, suggesting a multifaceted pathophysiological interaction. The identified causal links and mediation pathways underscore potential therapeutic targets, providing a foundation for interventions aimed at modulating immune responses to manage CRC.
{"title":"Causal effects and metabolites mediators between immune cell and risk of colorectal cancer: a Mendelian randomization study","authors":"Qian Yang, Bixia Duan, Jian Yue, Donglin Zhang, Xueping Chen, Mengjia Shi, Jie Kan, Ruochan Li, Hongda Li, Lin Gan","doi":"10.3389/fimmu.2024.1444222","DOIUrl":"https://doi.org/10.3389/fimmu.2024.1444222","url":null,"abstract":"ObjectiveThe involvement of immune cells in colorectal cancer (CRC) and their interplay with metabolic disorders are yet to be fully elucidated. This study examines how peripheral immune cells, inferred genetically, affect CRC and investigates the intermediary roles of metabolites.MethodsWe employed a two-sample bidirectional Mendelian randomization (MR) approach to assess the causal influence of immune cells on CRC. Additionally, a two-step MR strategy was utilized to pinpoint potential metabolites that mediate this effect. Our analysis incorporated data from genome-wide association studies (GWAS), involving 731 immune cell types, 1,400 metabolites, and CRC outcomes. The primary method of analysis was randomized inverse variance weighting (IVW), supported by MR-Egger, weighted median, simple mode, and weighted mode analyses. Sensitivity checks were conducted using Cochran’s Q test, MR-PRESSO test, MR-Egger regression intercept, and leave-one-out analysis.ResultsThe study identified 23 immune cell types and 17 metabolites that are causally linked to CRC. Our mediation analysis highlighted that nine metabolites act as intermediaries in the relationship between nine specific immune cells and CRC risk. Notably, The ratios of Adenosine 5’-monophosphate (AMP) to aspartate and Retinol (Vitamin A) to linoleoyl-arachidonoyl-glycerol (18:2 to 20:4) were found to concurrently mediate the promoting effects of Myeloid DC %DC and BAFF-R on B cells in colorectal cancer (CRC). Moreover, iminodiacetate (IDA) was found to mediate the protective effect of CD14<jats:sup>+</jats:sup> CD16<jats:sup>-</jats:sup> monocytes on CRC, contributing 11.8% to this mediation. In contrast, IDA was also seen to decrease the protective effect of IgD<jats:sup>+</jats:sup> CD38br %B cells on CRC risk, with a mediation effect proportion of -10.4%.ConclusionThis study delineates a complex network involving immune cells, metabolites, and CRC, suggesting a multifaceted pathophysiological interaction. The identified causal links and mediation pathways underscore potential therapeutic targets, providing a foundation for interventions aimed at modulating immune responses to manage CRC.","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142222510","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 : 2024-09-11DOI: 10.3389/fimmu.2024.1445555
Jiatong Li, Yang Bai, He Zhang, Ting Chen, Guanning Shang
IntroductionOsteosarcoma is a common type of bone cancer characterized by a poor prognosis due to its metastatic nature. The tumor microenvironment (TME) plays a critical role in tumor metastasis and therapy response. Therefore, our study aims to explore the metastatic mechanism of osteosarcoma, potentially opening new avenues for cancer treatment.MethodsIn this study, we collected data from the GSE152048, GSE14359, and GSE49003 datasets. Differentially expressed genes (DEGs) were identified in osteosarcoma cases with primary and metastatic features using R software and the limma package. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to investigate metastasis-related genes. A protein–protein interaction (PPI) network was established using the STRING database to further analyze these metastasis-associated genes. The abundances of different cell types with a mixed cell population were estimated using the CIBERSORT approach. The scRNA-seq data were analyzed by the Seurat package in R software, and intercellular communications were elucidated using the CellChat R package.ResultsIn this study, 92 DEGs related to metastasis were identified, including 41 upregulated and 51 downregulated genes in both the GSE14359 and GSE49003 datasets. Metastasis-associated pathways were identified, including those involving the cyclin-dependent protein kinase holoenzyme complex, transferase complex, transferring phosphorus-containing groups, SCF ubiquitin ligase complex, and the serine/threonine protein kinase complex. KEGG and PPI network analyses revealed 15 hub genes, including Skp2, KIF20A, CCNF, TROAP, PHB, CKS1B, MCM3, CCNA2, TRIP13, CENPM, Hsp90AB1, JUN, CKS2, TK1, and KIF4A. Skp2 has been known as an E3 ubiquitin ligase involved in osteosarcoma progression. The proportion of CD8+ T cells was found to be higher in metastatic osteosarcoma tissues, and high expression of PHB was associated with a favorable prognosis in osteosarcoma patients. Additionally, 23 cell clusters were classified into eight cell types, including chondrocytes, MSC, T cells, monocytes, tissue stem cells, neurons, endothelial cells, and macrophages. The 15 hub genes were expressed across various cell types, and interactions between different cell types were observed.ConclusionOur study reveals the intricate communication between tumor microenvironment components and tumor metastasis in osteosarcoma.
{"title":"Single-cell RNA sequencing reveals the communications between tumor microenvironment components and tumor metastasis in osteosarcoma","authors":"Jiatong Li, Yang Bai, He Zhang, Ting Chen, Guanning Shang","doi":"10.3389/fimmu.2024.1445555","DOIUrl":"https://doi.org/10.3389/fimmu.2024.1445555","url":null,"abstract":"IntroductionOsteosarcoma is a common type of bone cancer characterized by a poor prognosis due to its metastatic nature. The tumor microenvironment (TME) plays a critical role in tumor metastasis and therapy response. Therefore, our study aims to explore the metastatic mechanism of osteosarcoma, potentially opening new avenues for cancer treatment.MethodsIn this study, we collected data from the GSE152048, GSE14359, and GSE49003 datasets. Differentially expressed genes (DEGs) were identified in osteosarcoma cases with primary and metastatic features using R software and the limma package. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to investigate metastasis-related genes. A protein–protein interaction (PPI) network was established using the STRING database to further analyze these metastasis-associated genes. The abundances of different cell types with a mixed cell population were estimated using the CIBERSORT approach. The scRNA-seq data were analyzed by the Seurat package in R software, and intercellular communications were elucidated using the CellChat R package.ResultsIn this study, 92 DEGs related to metastasis were identified, including 41 upregulated and 51 downregulated genes in both the GSE14359 and GSE49003 datasets. Metastasis-associated pathways were identified, including those involving the cyclin-dependent protein kinase holoenzyme complex, transferase complex, transferring phosphorus-containing groups, SCF ubiquitin ligase complex, and the serine/threonine protein kinase complex. KEGG and PPI network analyses revealed 15 hub genes, including Skp2, KIF20A, CCNF, TROAP, PHB, CKS1B, MCM3, CCNA2, TRIP13, CENPM, Hsp90AB1, JUN, CKS2, TK1, and KIF4A. Skp2 has been known as an E3 ubiquitin ligase involved in osteosarcoma progression. The proportion of CD8+ T cells was found to be higher in metastatic osteosarcoma tissues, and high expression of PHB was associated with a favorable prognosis in osteosarcoma patients. Additionally, 23 cell clusters were classified into eight cell types, including chondrocytes, MSC, T cells, monocytes, tissue stem cells, neurons, endothelial cells, and macrophages. The 15 hub genes were expressed across various cell types, and interactions between different cell types were observed.ConclusionOur study reveals the intricate communication between tumor microenvironment components and tumor metastasis in osteosarcoma.","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142222515","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 : 2024-09-11DOI: 10.3389/fimmu.2024.1453740
Michael Benavidez Arias, An Nguyen, Daniel Ross, David Eagerton, Krit Ritthipichai
A robust T-cell expansion process involves co-culturing T-cells with non-proliferating feeder cells combined with anti-CD3 antibody and IL-2. Although ionizing irradiation effectively inhibits feeder cell proliferation, the high operating costs limit cell therapy research to well-funded institutions. UVC, known for causing DNA damage-induced cell death and commonly used for environmental sterilization, presents a cost-effective alternative to ionizing irradiation for generating non-proliferating feeder cells. UVC irradiation of K562 artificial antigen presenting cells (aAPCs) resulted in significant DNA damage, evidenced by increased γ-H2AX phosphorylation within 15 minutes and elevated 8-OHdG levels at 24 hours. This indicates the occurrence of DNA double-strand breaks and oxidative damage. Following UVC irradiation, glucose uptake and ATP production were significantly reduced, whereas aCD3 retention at the surface of the cell increased twofold. Selective inhibition of glucose uptake and ATP production similarly enhanced aCD3 retention by approximately 10-fold and 6-fold, respectively. This suggests that UVC-induced energy deprivation dampens aCD3 internalization, potentially enhancing T-cell activation through prolonged aCD3 and T-cell receptor interaction. Tumor-infiltrating lymphocytes (TILs) expanded with UVC-irradiated PBMCs demonstrated comparable viability, expansion, immunophenotype, and effector function to those expanded with ionizing irradiation. UVC irradiation was equally effective in suppressing feeder cell proliferation and facilitating the expansion of functionally potent T-cells compared to traditional ionizing irradiation. Implementing UVC irradiation in T-cell expansion can significantly reduce costs, enhancing the accessibility and feasibility of cell therapy research across various institutions.
强大的 T 细胞扩增过程包括将 T 细胞与不增殖的饲养细胞结合抗 CD3 抗体和 IL-2 共同培养。虽然电离辐照能有效抑制饲养细胞的增殖，但高昂的操作成本限制了资金雄厚的机构开展细胞疗法研究。众所周知，紫外线会导致 DNA 损伤引起的细胞死亡，常用于环境消毒，它是电离辐照的一种经济有效的替代方法，可用于生成不增殖的供体细胞。对 K562 人工抗原提呈细胞（aAPCs）进行紫外线照射会导致显著的 DNA 损伤，表现为 15 分钟内 γ-H2AX 磷酸化增加，24 小时后 8-OHdG 水平升高。这表明发生了 DNA 双链断裂和氧化损伤。经紫外线照射后，葡萄糖摄取和 ATP 生成显著减少，而 aCD3 在细胞表面的保留增加了两倍。选择性抑制葡萄糖摄取和 ATP 生成同样也会使 aCD3 的保留分别增加约 10 倍和 6 倍。这表明，紫外线诱导的能量剥夺抑制了 aCD3 的内化，有可能通过延长 aCD3 与 T 细胞受体的相互作用来增强 T 细胞的活化。用经紫外线照射的PBMCs扩增的肿瘤浸润淋巴细胞（TILs）在存活率、扩增、免疫表型和效应功能方面与电离照射扩增的TILs相当。与传统的电离照射相比，紫外线照射在抑制供养细胞增殖和促进功能强大的 T 细胞扩增方面同样有效。在 T 细胞扩增过程中使用紫外线辐照可大大降低成本，提高各机构细胞疗法研究的可及性和可行性。
{"title":"Lighting the way: an economical alternative to feeder cell Irradiation for T-cell expansion","authors":"Michael Benavidez Arias, An Nguyen, Daniel Ross, David Eagerton, Krit Ritthipichai","doi":"10.3389/fimmu.2024.1453740","DOIUrl":"https://doi.org/10.3389/fimmu.2024.1453740","url":null,"abstract":"A robust T-cell expansion process involves co-culturing T-cells with non-proliferating feeder cells combined with anti-CD3 antibody and IL-2. Although ionizing irradiation effectively inhibits feeder cell proliferation, the high operating costs limit cell therapy research to well-funded institutions. UVC, known for causing DNA damage-induced cell death and commonly used for environmental sterilization, presents a cost-effective alternative to ionizing irradiation for generating non-proliferating feeder cells. UVC irradiation of K562 artificial antigen presenting cells (aAPCs) resulted in significant DNA damage, evidenced by increased γ-H2AX phosphorylation within 15 minutes and elevated 8-OHdG levels at 24 hours. This indicates the occurrence of DNA double-strand breaks and oxidative damage. Following UVC irradiation, glucose uptake and ATP production were significantly reduced, whereas aCD3 retention at the surface of the cell increased twofold. Selective inhibition of glucose uptake and ATP production similarly enhanced aCD3 retention by approximately 10-fold and 6-fold, respectively. This suggests that UVC-induced energy deprivation dampens aCD3 internalization, potentially enhancing T-cell activation through prolonged aCD3 and T-cell receptor interaction. Tumor-infiltrating lymphocytes (TILs) expanded with UVC-irradiated PBMCs demonstrated comparable viability, expansion, immunophenotype, and effector function to those expanded with ionizing irradiation. UVC irradiation was equally effective in suppressing feeder cell proliferation and facilitating the expansion of functionally potent T-cells compared to traditional ionizing irradiation. Implementing UVC irradiation in T-cell expansion can significantly reduce costs, enhancing the accessibility and feasibility of cell therapy research across various institutions.","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142222536","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}
BackgroundImmune checkpoint inhibitor (ICI)-associated myocarditis is a rare, but potentially fatal, immune-related adverse event. Hence, identifying biomarkers is critical for selecting and managing patients receiving ICI treatment. Serum autoantibodies (AAbs) in patients with ICI myocarditis may serve as potential biomarkers for predicting, diagnosing, and prognosing ICI myocarditis. We conducted a pilot study using a human proteome microarray with approximately 17,000 unique full-length human proteins to investigate AAbs associated with ICI myocarditis.Methods and resultsAAb profiling was performed using sera collected from three patients with ICI myocarditis before the start of ICI treatment and immediately after myocarditis onset. All patients received anti-programmed death-1 antibody monotherapy. At baseline, 116, 296, and 154 autoantigens reacted positively to immunoglobulin G (IgG) in the serum samples from Cases 1, 2, and 3, respectively. Among these proteins, the recombination signal-binding protein for the immunoglobulin kappa J region (RBPJ) was recognized by all three samples, and 32 autoantigens were recognized by any two of the three samples. At the onset of ICI myocarditis, compared to baseline, 48, 114, and 5 autoantigens reacted more strongly with IgG in the serum samples from Cases 1, 2, and 3, respectively. Among these, antibodies against eukaryotic translation initiation factor 4E binding protein 3 (EIF4EBP3) were the most upregulated, with a 38-fold increase. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses highlighted that B-cell receptor signaling, leukocyte transendothelial migration, and thymus development were among the most affected pathways. Enrichment analyses using DisGeNET revealed that proteins reacting to AAbs detected in patients with ICI myocarditis are associated with several diseases, including dilated cardiomyopathy and muscle weakness.ConclusionsThis pilot study provides the first integrated analysis of serum AAb profiling in patients with ICI myocarditis and identifies novel candidate markers associated with an increased risk of developing ICI myocarditis and its pathogenesis. However, our results require further independent validation in clinical trials involving a larger number of patients.
{"title":"Autoantibody profiling of patients with immune checkpoint inhibitor-associated myocarditis: a pilot study","authors":"Siqi Li, DongZhu Xu, Nobuyuki Murakoshi, Zixun Yuan, Takuro Imaoka, Kazuko Tajiri","doi":"10.3389/fimmu.2024.1423622","DOIUrl":"https://doi.org/10.3389/fimmu.2024.1423622","url":null,"abstract":"BackgroundImmune checkpoint inhibitor (ICI)-associated myocarditis is a rare, but potentially fatal, immune-related adverse event. Hence, identifying biomarkers is critical for selecting and managing patients receiving ICI treatment. Serum autoantibodies (AAbs) in patients with ICI myocarditis may serve as potential biomarkers for predicting, diagnosing, and prognosing ICI myocarditis. We conducted a pilot study using a human proteome microarray with approximately 17,000 unique full-length human proteins to investigate AAbs associated with ICI myocarditis.Methods and resultsAAb profiling was performed using sera collected from three patients with ICI myocarditis before the start of ICI treatment and immediately after myocarditis onset. All patients received anti-programmed death-1 antibody monotherapy. At baseline, 116, 296, and 154 autoantigens reacted positively to immunoglobulin G (IgG) in the serum samples from Cases 1, 2, and 3, respectively. Among these proteins, the recombination signal-binding protein for the immunoglobulin kappa J region (RBPJ) was recognized by all three samples, and 32 autoantigens were recognized by any two of the three samples. At the onset of ICI myocarditis, compared to baseline, 48, 114, and 5 autoantigens reacted more strongly with IgG in the serum samples from Cases 1, 2, and 3, respectively. Among these, antibodies against eukaryotic translation initiation factor 4E binding protein 3 (EIF4EBP3) were the most upregulated, with a 38-fold increase. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses highlighted that B-cell receptor signaling, leukocyte transendothelial migration, and thymus development were among the most affected pathways. Enrichment analyses using DisGeNET revealed that proteins reacting to AAbs detected in patients with ICI myocarditis are associated with several diseases, including dilated cardiomyopathy and muscle weakness.ConclusionsThis pilot study provides the first integrated analysis of serum AAb profiling in patients with ICI myocarditis and identifies novel candidate markers associated with an increased risk of developing ICI myocarditis and its pathogenesis. However, our results require further independent validation in clinical trials involving a larger number of patients.","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142222446","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 : 2024-09-11DOI: 10.3389/fimmu.2024.1472133
Dongzhi Wang, Xinyu Weng, Wenhui Yue, Linlin Shang, Yidong Wei, John S. Clemmer, Yawei Xu, Yingjie Chen
IntroductionEven under the standard medical care, patients with left ventricular (LV) failure or heart failure (HF) often progress to pulmonary hypertension and right ventricular (RV) hypertrophy. We previously showed that inflammation and regulatory T cells (Tregs) modulate HF progression in mice with preexisting LV failure. The main objective of this study is to determine the role of CD8+ T cells in modulating LV failure and the consequent pulmonary inflammation and RV hypertrophy in mice with preexisting LV failure.MethodsMice with LV failure produced by transverse aortic constriction (TAC) were randomized to depletion of cytotoxic CD8+ T cells, Tregs, or both using specific blocking antibodies. Cardiac function, lung inflammation, fibrosis, vascular remodeling, and right ventricular remodeling were determined.ResultsLV failure caused pulmonary inflammation, fibrosis, vascular remodeling, and RV hypertrophy. Depletion of CD8+ T cells significantly attenuated above changes in mice with preexisting LV failure. LV failure was associated with increased CD4+ and CD8+ T cell activation, and increased ratios of activated T cells to Tregs. Treg depletion exacerbated lung inflammation and HF progression, as well as lung CD4+ and CD8+ T cell infiltration and activation in HF mice. However, CD8+ T cells depletion rescue these mice from exacerbated lung inflammation and RV hypertrophy after Treg depletion.DiscussionOur findings demonstrate an important role of CD8+ T cells in promoting pulmonary inflammation and RV hypertrophy in mice with preexisting LV failure. Depletion of CD8+ T cells also rescued HF mice from the exacerbated HF progression by Treg depletion.
导言即使在标准的医疗护理下，左心室衰竭或心力衰竭（HF）患者也常常会发展为肺动脉高压和右心室肥大。我们以前的研究表明，炎症和调节性 T 细胞（Tregs）可调节已存在左心室衰竭的小鼠的 HF 进展。本研究的主要目的是确定 CD8+ T 细胞在调节左心室衰竭以及由此引起的肺部炎症和左心室肥大中的作用。方法：使用特异性阻断抗体随机清除横主动脉收缩（TAC）导致左心室衰竭的小鼠的细胞毒性 CD8+ T 细胞、Tregs 或两者。结果左心室衰竭导致肺部炎症、纤维化、血管重塑和右心室肥大。对已存在左心室衰竭的小鼠而言，消耗 CD8+ T 细胞可显著减轻上述变化。左心室衰竭与 CD4+ 和 CD8+ T 细胞活化增加以及活化 T 细胞与 Tregs 比率增加有关。Treg消耗会加剧肺部炎症和HF进展，以及HF小鼠肺部CD4+和CD8+ T细胞的浸润和活化。我们的研究结果表明，CD8+ T 细胞在促进已有左心室功能衰竭的小鼠肺部炎症和左心室肥大中发挥了重要作用。我们的研究结果表明，CD8+ T 细胞在促进已有左心室衰竭的小鼠肺部炎症和 RV 肥厚中发挥了重要作用。
{"title":"CD8 T cells promote heart failure progression in mice with preexisting left ventricular dysfunction","authors":"Dongzhi Wang, Xinyu Weng, Wenhui Yue, Linlin Shang, Yidong Wei, John S. Clemmer, Yawei Xu, Yingjie Chen","doi":"10.3389/fimmu.2024.1472133","DOIUrl":"https://doi.org/10.3389/fimmu.2024.1472133","url":null,"abstract":"IntroductionEven under the standard medical care, patients with left ventricular (LV) failure or heart failure (HF) often progress to pulmonary hypertension and right ventricular (RV) hypertrophy. We previously showed that inflammation and regulatory T cells (Tregs) modulate HF progression in mice with preexisting LV failure. The main objective of this study is to determine the role of CD8<jats:sup>+</jats:sup> T cells in modulating LV failure and the consequent pulmonary inflammation and RV hypertrophy in mice with preexisting LV failure.MethodsMice with LV failure produced by transverse aortic constriction (TAC) were randomized to depletion of cytotoxic CD8<jats:sup>+</jats:sup> T cells, Tregs, or both using specific blocking antibodies. Cardiac function, lung inflammation, fibrosis, vascular remodeling, and right ventricular remodeling were determined.ResultsLV failure caused pulmonary inflammation, fibrosis, vascular remodeling, and RV hypertrophy. Depletion of CD8<jats:sup>+</jats:sup> T cells significantly attenuated above changes in mice with preexisting LV failure. LV failure was associated with increased CD4<jats:sup>+</jats:sup> and CD8<jats:sup>+</jats:sup> T cell activation, and increased ratios of activated T cells to Tregs. Treg depletion exacerbated lung inflammation and HF progression, as well as lung CD4<jats:sup>+</jats:sup> and CD8<jats:sup>+</jats:sup> T cell infiltration and activation in HF mice. However, CD8<jats:sup>+</jats:sup> T cells depletion rescue these mice from exacerbated lung inflammation and RV hypertrophy after Treg depletion.DiscussionOur findings demonstrate an important role of CD8<jats:sup>+</jats:sup> T cells in promoting pulmonary inflammation and RV hypertrophy in mice with preexisting LV failure. Depletion of CD8<jats:sup>+</jats:sup> T cells also rescued HF mice from the exacerbated HF progression by Treg depletion.","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142222381","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 : 2024-09-11DOI: 10.3389/fimmu.2024.1441994
Laura E. Martínez, Begoña Comin-Anduix, Miriam Güemes-Aragon, Javier Ibarrondo, Roger Detels, Matthew J. Mimiaga, Marta Epeldegui
People living with HIV (PLWH) are at higher risk of developing lymphoma. In this study, we performed cytometry by time-of-flight (CyTOF) on peripheral blood mononuclear cells of cART-naïve HIV+ individuals and cART-naïve HIV+ individuals prior to AIDS-associated non-Hodgkin lymphoma (pre-NHL) diagnosis. Participants were enrolled in the Los Angeles site of the MACS/WIHS Combined Cohort Study (MWCCS). Uniform Manifold Approximation and Projection (UMAP) and unsupervised clustering analysis were performed to identify differences in the expression of B-cell activation markers and/or oncogenic markers associated with lymphomagenesis. CD10+CD27- B cells, CD20+CD27- B cells, and B-cell populations with aberrant features (CD20+CD27+CXCR4+CD71+ B cells and CD20+CXCR4+cMYC+ B cells) were significantly elevated in HIV+ cART-naïve compared to HIV-negative samples. CD20+CD27+CD24+CXCR4+CXCR5+ B cells, CD20+CD27+CD10+CD24+CXCR4+cMYC+ B cells, and a cluster of CD20+CXCR4hiCD27-CD24+CXCR5+CD40+CD4+AICDA+ B cells were significantly elevated in HIV+ pre-NHL (cART-naïve) compared to HIV+ cART-naïve samples. A potentially clonal cluster of CD20+CXCR4+CXCR5+cMYC+AICDA+ B cells and a cluster of germinal center B-cell-like cells (CD19-CD20+CXCR4+Bcl-6+PD-L1+cMYC+) were also found in the circulation of HIV+ pre-NHL (cART-naïve) samples. Moreover, significantly elevated clusters of CD19+CD24hiCD38hi cMYC+ AICDA+ B regulatory cells were identified in HIV+ pre-NHL (cART-naïve) compared to HIV+ cART-naïve samples. The present study identifies unique B-cell subsets in PLWH with potential pre-malignant features that may contribute to the development of pre-tumor B cells in PLWH and that may play a role in lymphomagenesis.
{"title":"Characterization of unique B-cell populations in the circulation of people living with HIV prior to non-Hodgkin lymphoma diagnosis","authors":"Laura E. Martínez, Begoña Comin-Anduix, Miriam Güemes-Aragon, Javier Ibarrondo, Roger Detels, Matthew J. Mimiaga, Marta Epeldegui","doi":"10.3389/fimmu.2024.1441994","DOIUrl":"https://doi.org/10.3389/fimmu.2024.1441994","url":null,"abstract":"People living with HIV (PLWH) are at higher risk of developing lymphoma. In this study, we performed cytometry by time-of-flight (CyTOF) on peripheral blood mononuclear cells of cART-naïve HIV+ individuals and cART-naïve HIV+ individuals prior to AIDS-associated non-Hodgkin lymphoma (pre-NHL) diagnosis. Participants were enrolled in the Los Angeles site of the MACS/WIHS Combined Cohort Study (MWCCS). Uniform Manifold Approximation and Projection (UMAP) and unsupervised clustering analysis were performed to identify differences in the expression of B-cell activation markers and/or oncogenic markers associated with lymphomagenesis. CD10<jats:sup>+</jats:sup>CD27<jats:sup>-</jats:sup> B cells, CD20<jats:sup>+</jats:sup>CD27<jats:sup>-</jats:sup> B cells, and B-cell populations with aberrant features (CD20<jats:sup>+</jats:sup>CD27<jats:sup>+</jats:sup>CXCR4<jats:sup>+</jats:sup>CD71<jats:sup>+</jats:sup> B cells and CD20<jats:sup>+</jats:sup>CXCR4<jats:sup>+</jats:sup>cMYC<jats:sup>+</jats:sup> B cells) were significantly elevated in HIV+ cART-naïve compared to HIV-negative samples. CD20<jats:sup>+</jats:sup>CD27<jats:sup>+</jats:sup>CD24<jats:sup>+</jats:sup>CXCR4<jats:sup>+</jats:sup>CXCR5<jats:sup>+</jats:sup> B cells, CD20<jats:sup>+</jats:sup>CD27<jats:sup>+</jats:sup>CD10<jats:sup>+</jats:sup>CD24<jats:sup>+</jats:sup>CXCR4<jats:sup>+</jats:sup>cMYC<jats:sup>+</jats:sup> B cells, and a cluster of CD20<jats:sup>+</jats:sup>CXCR4<jats:sup>hi</jats:sup>CD27<jats:sup>-</jats:sup>CD24<jats:sup>+</jats:sup>CXCR5<jats:sup>+</jats:sup>CD40<jats:sup>+</jats:sup>CD4<jats:sup>+</jats:sup>AICDA<jats:sup>+</jats:sup> B cells were significantly elevated in HIV+ pre-NHL (cART-naïve) compared to HIV+ cART-naïve samples. A potentially clonal cluster of CD20<jats:sup>+</jats:sup>CXCR4<jats:sup>+</jats:sup>CXCR5<jats:sup>+</jats:sup>cMYC<jats:sup>+</jats:sup>AICDA<jats:sup>+</jats:sup> B cells and a cluster of germinal center B-cell-like cells (CD19<jats:sup>-</jats:sup>CD20<jats:sup>+</jats:sup>CXCR4<jats:sup>+</jats:sup>Bcl-6<jats:sup>+</jats:sup>PD-L1<jats:sup>+</jats:sup>cMYC<jats:sup>+</jats:sup>) were also found in the circulation of HIV+ pre-NHL (cART-naïve) samples. Moreover, significantly elevated clusters of CD19<jats:sup>+</jats:sup>CD24<jats:sup>hi</jats:sup>CD38<jats:sup>hi</jats:sup> cMYC<jats:sup>+</jats:sup> AICDA<jats:sup>+</jats:sup> B regulatory cells were identified in HIV+ pre-NHL (cART-naïve) compared to HIV+ cART-naïve samples. The present study identifies unique B-cell subsets in PLWH with potential pre-malignant features that may contribute to the development of pre-tumor B cells in PLWH and that may play a role in lymphomagenesis.","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142222417","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 : 2024-09-11DOI: 10.3389/fimmu.2024.1445530
Liangjun Zhang, Huixiu Zhong, Jiwen Fan, Jiansen Mao, Yi Li
BackgroundT helper (Th) cell subsets primarily assist B cells in differentiating into plasma cells in the germinal center. The mechanism of malignant transformation of plasma cells is an important target for the clinical treatment of MM; however, the mechanism remains unclear.MethodsWe collected the peripheral blood (PB) and bone marrow (BM) samples of 33 patients with MM. In addition, the PB was also collected from 25 normal healthy controls (HCs). We analyzed the percentages of Th cell subsets in the PB and BM samples of patients with MM.ResultsTfh/CD4+ were positively correlated with the proportion of myeloma cells in the BM and PB samples (r = 0.592, P = 0.002 and r = 0.510, P = 0.010 respectively), and showed a strong correlation between the BM and PB samples (r = 0.6559, P = 0.0095). In the PB samples, the percentages of Th2/CD4+ and Tfh2/Tfh cells were significantly lower in patients with MM than in HCs (P = 0.00013 and P = 0.0004, respectively), whereas the percentage of Th17/CD4+ and Tfh17/Tfh was significantly higher in newly diagnosed patients with MM than in HCs (P = 0.0037 and P = 0.03, respectively), and all these cells showed a good predictive value for MM (area under the curve [AUC] 0.781, = 0.792, = 0.837, and 0.723 respectively). In the PB samples, all subsets of PD-1+ICOS- Tfh showed a noticeable downward trend in MM from newly diagnosed to non-remission and remission groups. In contrast, all subsets of PD-1-ICOS+ Tfh increased gradually.ConclusionTh cell subsets play an important role in the occurrence and development of MM and may provide a fundamental basis for identifying new immunotherapy targets and prognosis.
背景T辅助细胞亚群主要协助B细胞在生殖中心分化为浆细胞。浆细胞恶性转化的机制是 MM 临床治疗的一个重要靶点；然而，其机制仍不清楚。方法我们收集了 33 名 MM 患者的外周血（PB）和骨髓（BM）样本。此外，我们还采集了 25 名正常健康对照者（HCs）的外周血样本。结果Tfh/CD4+与骨髓和外周血样本中骨髓瘤细胞的比例呈正相关（分别为r = 0.592，P = 0.002和r = 0.510，P = 0.010），并且在骨髓和外周血样本之间显示出很强的相关性（r = 0.6559，P = 0.0095）。在肺结核样本中，MM 患者的 Th2/CD4+ 和 Tfh2/Tfh 细胞百分比显著低于 HCs（分别为 P = 0.00013 和 P = 0.0004），而新诊断的 MM 患者的 Th17/CD4+ 和 Tfh17/Tfh 百分比显著高于 HCs（分别为 P = 0.0037 和 P = 0.03），而且所有这些细胞对 MM 都有很好的预测价值（曲线下面积 [AUC] 分别为 0.781、= 0.792、= 0.837 和 0.723）。在 PB 样本中，PD-1+ICOS- Tfh 的所有亚群在 MM 新诊断组、非缓解组和缓解组中都显示出明显的下降趋势。结论Th 细胞亚群在 MM 的发生和发展中起着重要作用，可为确定新的免疫治疗靶点和预后提供基本依据。
{"title":"Clinical significance of T helper cell subsets in the peripheral blood and bone marrow of patients with multiple myeloma","authors":"Liangjun Zhang, Huixiu Zhong, Jiwen Fan, Jiansen Mao, Yi Li","doi":"10.3389/fimmu.2024.1445530","DOIUrl":"https://doi.org/10.3389/fimmu.2024.1445530","url":null,"abstract":"BackgroundT helper (Th) cell subsets primarily assist B cells in differentiating into plasma cells in the germinal center. The mechanism of malignant transformation of plasma cells is an important target for the clinical treatment of MM; however, the mechanism remains unclear.MethodsWe collected the peripheral blood (PB) and bone marrow (BM) samples of 33 patients with MM. In addition, the PB was also collected from 25 normal healthy controls (HCs). We analyzed the percentages of Th cell subsets in the PB and BM samples of patients with MM.ResultsTfh/CD4<jats:sup>+</jats:sup> were positively correlated with the proportion of myeloma cells in the BM and PB samples (r = 0.592, P = 0.002 and r = 0.510, P = 0.010 respectively), and showed a strong correlation between the BM and PB samples (r = 0.6559, P = 0.0095). In the PB samples, the percentages of Th2/CD4<jats:sup>+</jats:sup> and Tfh2/Tfh cells were significantly lower in patients with MM than in HCs (P = 0.00013 and P = 0.0004, respectively), whereas the percentage of Th17/CD4<jats:sup>+</jats:sup> and Tfh17/Tfh was significantly higher in newly diagnosed patients with MM than in HCs (P = 0.0037 and P = 0.03, respectively), and all these cells showed a good predictive value for MM (area under the curve [AUC] 0.781, = 0.792, = 0.837, and 0.723 respectively). In the PB samples, all subsets of PD-1<jats:sup>+</jats:sup>ICOS<jats:sup>-</jats:sup> Tfh showed a noticeable downward trend in MM from newly diagnosed to non-remission and remission groups. In contrast, all subsets of PD-1<jats:sup>-</jats:sup>ICOS<jats:sup>+</jats:sup> Tfh increased gradually.ConclusionTh cell subsets play an important role in the occurrence and development of MM and may provide a fundamental basis for identifying new immunotherapy targets and prognosis.","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142222530","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 : 2024-09-11DOI: 10.3389/fimmu.2024.1448780
Julio A. Huapaya, Salina Gairhe, Shreya Kanth, Xin Tian, Cumhur Y. Demirkale, David Regenold, Jian Sun, Nicolas F. Lynch, Renjie Luo, Alisa Forsberg, Robin Dewar, Tauseef Rehman, Willy Li, Janell Krack, Janaki Kuruppu, Etsubdink A. Aboye, Christopher Barnett, Jeffrey R. Strich, Richard Davey, Richard Childs, Daniel Chertow, Joseph A. Kovacs, Parizad Torabi-Parizi, Anthony F. Suffredini
BackgroundLimited data are available describing the effects of SARS-CoV-2 breakthrough infections on the plasma proteome.MethodsPCR-positive SARS-CoV-2 patients, enrolled in a natural history study, underwent analysis of the plasma proteome. A prospective cohort of 66 unvaccinated and 24 vaccinated persons with different degrees of infection severity were evaluated acutely (within 40 days of symptom onset), and at three and ten months. Comparisons based on vaccination status alone and unsupervised hierarchical clustering were performed. A second cohort of vaccinated Omicron patients were evaluated acutely and at ten months.ResultsAcutely, unvaccinated patients manifested overexpression of proteins involved in immune and inflammatory responses, while vaccinated patients exhibited adaptive immune responses without significant inflammation. At three and ten months, only unvaccinated patients had diminished but sustained inflammatory (C3b, CCL15, IL17RE) and immune responses (DEFA5,TREM1). Both groups had underexpression of pathways essential for cellular function, signaling, and angiogenesis (AKT1, MAPK14, HSPB1) across phases. Unsupervised clustering, based on protein expression, identified four groups of patients with variable vaccination rates demonstrating that additional clinical factors influence the plasma proteome. The proteome of vaccinated Omicron patients did not differ from vaccinated pre-Omicron patients.ConclusionsVaccination attenuates the inflammatory response to SARS-CoV-2 infection across phases. However, at ten months after symptom onset, changes in the plasma proteome persist in both vaccinated and unvaccinated individuals, which may be relevant to post-acute sequelae of SARS-CoV-2 and other viral infections associated with post-acute infection syndromes.
{"title":"Alterations in the plasma proteome persist ten months after recovery from mild to moderate SARS-CoV-2 infection","authors":"Julio A. Huapaya, Salina Gairhe, Shreya Kanth, Xin Tian, Cumhur Y. Demirkale, David Regenold, Jian Sun, Nicolas F. Lynch, Renjie Luo, Alisa Forsberg, Robin Dewar, Tauseef Rehman, Willy Li, Janell Krack, Janaki Kuruppu, Etsubdink A. Aboye, Christopher Barnett, Jeffrey R. Strich, Richard Davey, Richard Childs, Daniel Chertow, Joseph A. Kovacs, Parizad Torabi-Parizi, Anthony F. Suffredini","doi":"10.3389/fimmu.2024.1448780","DOIUrl":"https://doi.org/10.3389/fimmu.2024.1448780","url":null,"abstract":"BackgroundLimited data are available describing the effects of SARS-CoV-2 breakthrough infections on the plasma proteome.MethodsPCR-positive SARS-CoV-2 patients, enrolled in a natural history study, underwent analysis of the plasma proteome. A prospective cohort of 66 unvaccinated and 24 vaccinated persons with different degrees of infection severity were evaluated acutely (within 40 days of symptom onset), and at three and ten months. Comparisons based on vaccination status alone and unsupervised hierarchical clustering were performed. A second cohort of vaccinated Omicron patients were evaluated acutely and at ten months.ResultsAcutely, unvaccinated patients manifested overexpression of proteins involved in immune and inflammatory responses, while vaccinated patients exhibited adaptive immune responses without significant inflammation. At three and ten months, only unvaccinated patients had diminished but sustained inflammatory (C3b, CCL15, IL17RE) and immune responses (DEFA5,TREM1). Both groups had underexpression of pathways essential for cellular function, signaling, and angiogenesis (AKT1, MAPK14, HSPB1) across phases. Unsupervised clustering, based on protein expression, identified four groups of patients with variable vaccination rates demonstrating that additional clinical factors influence the plasma proteome. The proteome of vaccinated Omicron patients did not differ from vaccinated pre-Omicron patients.ConclusionsVaccination attenuates the inflammatory response to SARS-CoV-2 infection across phases. However, at ten months after symptom onset, changes in the plasma proteome persist in both vaccinated and unvaccinated individuals, which may be relevant to post-acute sequelae of SARS-CoV-2 and other viral infections associated with post-acute infection syndromes.","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142222533","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}
In the recent history of the SARS-CoV-2 outbreak, vaccines have been a crucial public health tool, playing a significant role in effectively preventing infections. However, improving the efficacy while minimizing side effects remains a major challenge. In recent years, there has been growing interest in nanoparticle-based delivery systems aimed at improving antigen delivery efficiency and immunogenicity. Among these, self-assembled nanoparticles with varying sizes, shapes, and surface properties have garnered considerable attention. This paper reviews the latest advancements in the design and development of SARS-CoV-2 vaccines utilizing self-assembled materials, highlighting their advantages in delivering viral immunogens. In addition, we briefly discuss strategies for designing a broad-spectrum universal vaccine, which provides insights and ideas for dealing with possible future infectious sarbecoviruses.
{"title":"Strategies for developing self-assembled nanoparticle vaccines against SARS-CoV-2 infection","authors":"Kaiwen Yang, Youqin Zeng, Xinyu Wu, Jia Li, Jinlin Guo","doi":"10.3389/fimmu.2024.1392898","DOIUrl":"https://doi.org/10.3389/fimmu.2024.1392898","url":null,"abstract":"In the recent history of the SARS-CoV-2 outbreak, vaccines have been a crucial public health tool, playing a significant role in effectively preventing infections. However, improving the efficacy while minimizing side effects remains a major challenge. In recent years, there has been growing interest in nanoparticle-based delivery systems aimed at improving antigen delivery efficiency and immunogenicity. Among these, self-assembled nanoparticles with varying sizes, shapes, and surface properties have garnered considerable attention. This paper reviews the latest advancements in the design and development of SARS-CoV-2 vaccines utilizing self-assembled materials, highlighting their advantages in delivering viral immunogens. In addition, we briefly discuss strategies for designing a broad-spectrum universal vaccine, which provides insights and ideas for dealing with possible future infectious sarbecoviruses.","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142222512","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}
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