Journal of immunology最新文献_第8页

RTF1 mediates epigenetic control of Th17 cell differentiation via H2B monoubiquitination. RTF1通过H2B单泛素化介导Th17细胞分化的表观遗传控制。

IF 3.6 3区医学

Journal of immunology Pub Date : 2025-02-24 DOI: 10.1093/jimmun/vkae043

Carolina Galan, Guangqing Lu, Richard Gill, Dun Li, Yifang Liu, Jun R Huh, Saiyu Hang

引用次数: 0

Differential shaping of T cell responses elicited by heterologous ChAd68/self-amplifying mRNA SIV vaccine in macaques in combination with αCTLA4, αPD-1, or FLT3R agonist. 异源ChAd68/自扩增mRNA SIV疫苗联合αCTLA4、αPD-1或FLT3R激动剂诱导猕猴T细胞反应的差异形成

IF 3.6 3区医学

Journal of immunology Pub Date : 2025-02-23 DOI: 10.1093/jimmun/vkae052

Amy R Rappaport, Elena Bekerman, Gregory R Boucher, Janette Sung, Brian Carr, Cesar A Corzo, Heather Larson, Melissa A Kachura, Ciaran D Scallan, Romas Geleziunas, Devi SenGupta, Karin Jooss

{"title":"Differential shaping of T cell responses elicited by heterologous ChAd68/self-amplifying mRNA SIV vaccine in macaques in combination with αCTLA4, αPD-1, or FLT3R agonist.","authors":"Amy R Rappaport, Elena Bekerman, Gregory R Boucher, Janette Sung, Brian Carr, Cesar A Corzo, Heather Larson, Melissa A Kachura, Ciaran D Scallan, Romas Geleziunas, Devi SenGupta, Karin Jooss","doi":"10.1093/jimmun/vkae052","DOIUrl":"https://doi.org/10.1093/jimmun/vkae052","url":null,"abstract":"While therapeutic vaccines are a promising strategy for inducing human immunodeficiency virus (HIV) control, HIV vaccines tested to date have offered limited benefit to people living with HIV. The barriers to success may include the use of vaccine platforms and/or immunogens that drive weak or suboptimal immune responses, immune escape and/or immune dysfunction associated with chronic infection despite effective antiretroviral therapy. Combining vaccines with immune modulators in a safe manner may address some of the challenges and thus increase the efficacy of therapeutic HIV vaccines. We evaluated the immunogenicity of a ChAd68/samRNA-based simian immunodeficiency virus (SIV) vaccine regimen alone and in combination with a series of immune modulators in a preclinical rhesus macaque (M. mulatta) model. The vaccine was co-delivered with the checkpoint inhibitors αPD-1 or αCTLA-4, or with a FLT3 receptor agonist (FLT3Ra) shown to differentiate and expand dendritic cells and improve T cell priming. We demonstrate that the magnitude, breadth and functionality of SIV-specific vaccine-elicited CD8+ T cell responses were enhanced by combination with either αPD-1, αCTLA-4, or FLT3Ra. Combination with FLT3Ra also expanded polyfunctional CD4+ T cell responses. Our data demonstrate enhanced and distinct shaping of vaccine-elicited immune responses by immune modulators with implications for developing a functional HIV cure.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

MyD88 determines T cell fate through BCAP-PI3K signaling. MyD88通过BCAP-PI3K信号决定T细胞命运。

IF 3.6 3区医学

Journal of immunology Pub Date : 2025-02-23 DOI: 10.1093/jimmun/vkae037

Abraham L Bayer, Zoie Magri, Hayley Muendlein, Alexander Poltorak, Pilar Alcaide

{"title":"MyD88 determines T cell fate through BCAP-PI3K signaling.","authors":"Abraham L Bayer, Zoie Magri, Hayley Muendlein, Alexander Poltorak, Pilar Alcaide","doi":"10.1093/jimmun/vkae037","DOIUrl":"10.1093/jimmun/vkae037","url":null,"abstract":"The life cycle of effector T cells is determined by signals downstream of the T cell receptor (TCR) that induce activation and proinflammatory activity, or death as part of the process to resolve inflammation. We recently reported that T cell myeloid differentiation primary response 88 (MyD88) tunes down TCR activation and limits T cell survival in the cardiac and tumor inflammatory environments, in contrast to its proinflammatory role in myeloid cells upon toll-like receptor (TLR) recognition of pathogen- and damage-associated molecular patterns. However, the molecular mechanism remains unknown. Here, we report a central regulatory role for MyD88 in T cell apoptosis after TCR activation and Fas ligation through an association with the B cell adaptor for phosphoinositide 3-kinase (B cell activating protein [BCAP]). We show that TCR engagement upregulates MyD88 and BCAP and promotes their interaction, thereby limiting availability of BCAP for downstream TCR-BCAP-PI3K-AKT signaling required for T cell activation and survival, which are enhanced in MyD88-/- activated T cells. Further, MyD88 and BCAP association and localization to the TCR was prevented by lipopolysaccharide (LPS) activation of TLR4 and restored T cell survival in wild-type cells. The enhanced T cell activation markers, proinflammatory signals, and survival advantage observed in MyD88-/- T cells was fully eliminated upon BCAP knockdown in T cells. Our data demonstrate that MyD88 acts downstream of the TCR to regulate T cell fate through its association with BCAP and elucidate a novel molecular mechanism for MyD88 in T cell biology that could be targeted to fine-tune T cell effector function and survival therapeutically.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11952871/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

General and individualized changes in T cell immunity during aging. 衰老过程中T细胞免疫的一般和个体化变化。

IF 3.6 3区医学

Journal of immunology Pub Date : 2025-02-15 DOI: 10.1093/jimmun/vkae033

Nianbin Song, Mostafa A Elbahnasawy, Nan-Ping Weng

引用次数: 0

Gene-modified NK cells expressing CD64 and preloaded with HIV-specific BNAbs target autologous HIV-1-infected CD4+ T cells by ADCC. 表达CD64的基因修饰NK细胞和预加载hiv特异性BNAbs通过ADCC靶向自体hiv -1感染的CD4+ T细胞。

IF 3.6 3区医学

Journal of immunology Pub Date : 2025-02-01 DOI: 10.1093/jimmun/vkae028

Costin Tomescu, Adiana Ochoa-Ortiz, Lily D Lu, Hong Kong, James L Riley, Luis J Montaner

{"title":"Gene-modified NK cells expressing CD64 and preloaded with HIV-specific BNAbs target autologous HIV-1-infected CD4+ T cells by ADCC.","authors":"Costin Tomescu, Adiana Ochoa-Ortiz, Lily D Lu, Hong Kong, James L Riley, Luis J Montaner","doi":"10.1093/jimmun/vkae028","DOIUrl":"10.1093/jimmun/vkae028","url":null,"abstract":"Natural killer (NK) cells can efficiently mediate antibody-dependent cellular cytotoxicity (ADCC) of antibody coated target cells via the low-affinity Fc-receptor, CD16, but cannot retain antibodies over time. To increase antibody retention and facilitate targeted ADCC, we genetically modified human NK cells with the high-affinity Fc receptor, CD64, so that we could preload them with HIV-specific broadly neutralizing antibodies (BNAbs) and enhance their capacity to target HIV-infected cells via ADCC. Purified NK cells from the peripheral blood of control donors or persons living with HIV were activated with interleukin (IL)-2/IL-15/IL-21 cytokines and transduced with a lentivirus encoding CD64. High levels of CD64 surface expression were maintained for multiple weeks on NK cells and CD64-transduced NK cells were phenotypically similar to control NK cells with strong expression of CD56, CD16, NKG2A, NKp46, CD69, HLA-DR, CD38, and CD57. CD64-transduced NK cells exhibited significantly greater capacity to bind HIV-specific BNAbs in short-term antibody binding assay as well as retain the BNAbs over time (1-wk antibody retention assay) compared with control NK cells only expressing CD16. BNAb-preloaded CD64-transduced NK cells showed a significantly enhanced capacity to mediate ADCC against autologous HIV-1-infected CD4+ primary T cells in both a short-term 4 h degranulation assay as well as a 24 h HIV p24 HIV elimination assay when compared with control NK cells. A chimeric CD64 enhanced NK cell strategy (NuKEs [NK Enhancement Strategy]) retaining bound HIV-specific BNAbs represents a novel autologous primary NK cell immunotherapy strategy against HIV through targeted ADCC.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"214 2","pages":"253-264"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878998/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effects of PARP1 inhibitor PJ-34 on TGFα, IL-6, and IL-1β levels in diabetic nephropathy. PARP1抑制剂PJ-34对糖尿病肾病患者TGFα、IL-6和IL-1β水平的影响

IF 3.6 3区医学

Journal of immunology Pub Date : 2025-02-01 DOI: 10.1093/jimmun/vkae024

Jing Ke, Yanan Fan, Shaochun Zhang

{"title":"Effects of PARP1 inhibitor PJ-34 on TGFα, IL-6, and IL-1β levels in diabetic nephropathy.","authors":"Jing Ke, Yanan Fan, Shaochun Zhang","doi":"10.1093/jimmun/vkae024","DOIUrl":"https://doi.org/10.1093/jimmun/vkae024","url":null,"abstract":"Diabetic nephropathy is a severe chronic complication characterized by cytotoxicity, inflammation, and fibrosis, ultimately leading to renal failure. This study systematically investigated the effects of the PARP1 inhibitor PJ-34 on high glucose-induced cytotoxicity, inflammation, and fibrosis in HK-2 cells, as well as its improvement on neuropathic pain response and transforming growth factor β (TGFβ) expression in a type 1 diabetes mellitus diabetic nephropathy mouse model. Through cellular and animal experiments, we observed that PJ-34 significantly enhanced the proliferative capacity of cells damaged by high glucose, reduced apoptosis, and decreased the release of proinflammatory factors TGFα, interleukin-6, and interleukin-1β. In the type 1 diabetes mellitus nephropathy mouse model, the administration of PJ-34 substantially improved parameters of neuropathic pain, alleviated renal tissue damage, reduced indicators of renal functional impairment-inhibited renal fibrosis, and reduced the key protein expression in the epithelial-mesenchymal transition process, acting through the regulation of the TGFβ/Smads signaling pathway. This study elucidated the mechanism of action of the PARP1 inhibitor PJ-34 as a potential therapeutic agent for diabetic nephropathy, offering a novel strategy for its treatment.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"214 2","pages":"304-315"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Aggregatin is a mitochondrial regulator of MAVS activation to drive innate immunity. 聚集蛋白是MAVS激活的线粒体调节因子，以驱动先天免疫。

IF 3.6 3区医学

Journal of immunology Pub Date : 2025-02-01 DOI: 10.1093/jimmun/vkae019

Ju Gao, Mao Ding, Yanbin Xiyang, Siyue Qin, Devanshi Shukla, Jiawei Xu, Masaru Miyagi, Hisashi Fujioka, Jingjing Liang, Xinglong Wang

{"title":"Aggregatin is a mitochondrial regulator of MAVS activation to drive innate immunity.","authors":"Ju Gao, Mao Ding, Yanbin Xiyang, Siyue Qin, Devanshi Shukla, Jiawei Xu, Masaru Miyagi, Hisashi Fujioka, Jingjing Liang, Xinglong Wang","doi":"10.1093/jimmun/vkae019","DOIUrl":"10.1093/jimmun/vkae019","url":null,"abstract":"Mitochondrial antiviral-signaling protein (MAVS) is a key adapter protein required for inducing type I interferons (IFN-Is) and other antiviral effector molecules. The formation of MAVS aggregates on mitochondria is essential for its activation; however, the regulatory mitochondrial factor that mediates the aggregation process is unknown. Our recent work has identified the protein Aggregatin as a critical seeding factor for β-amyloid peptide aggregation. Here we show that Aggregatin serves as a cross-seed for MAVS aggregates on mitochondria to orchestrate innate immune signaling. Aggregatin is primarily localized to mitochondria in the cytosol and has the ability to induce MAVS aggregation and MAVS-dependent IFN-I responses alone in both HEK293 cells and human leukemia monocytic THP-1 cells. Mitochondrial Aggregatin level increases upon viral infection. Also, Aggregatin knockout suppresses viral infection-induced MAVS aggregation and IFN-I signal cascade activation. Nemo-like kinase is further identified as a kinase phosphorylating Aggregatin at Ser59 to regulate its stability and cross-seeding activity. Collectively, our finding reveals an important physiological function of Aggregatin in innate immunity by cross-seeding MAVS aggregation.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"214 2","pages":"238-252"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Innateness transcriptome gradients characterize mouse T lymphocyte populations. 先天转录组梯度表征小鼠T淋巴细胞群。

IF 3.6 3区医学

Journal of immunology Pub Date : 2025-02-01 DOI: 10.1093/jimmun/vkae015

Gabriel Ascui, Viankail Cedillo-Castelan, Alba Mendis, Eleni Phung, Hsin-Yu Liu, Greet Verstichel, Shilpi Chandra, Mallory Paynich Murray, Cindy Luna, Hilde Cheroutre, Mitchell Kronenberg

{"title":"Innateness transcriptome gradients characterize mouse T lymphocyte populations.","authors":"Gabriel Ascui, Viankail Cedillo-Castelan, Alba Mendis, Eleni Phung, Hsin-Yu Liu, Greet Verstichel, Shilpi Chandra, Mallory Paynich Murray, Cindy Luna, Hilde Cheroutre, Mitchell Kronenberg","doi":"10.1093/jimmun/vkae015","DOIUrl":"10.1093/jimmun/vkae015","url":null,"abstract":"A fundamental dichotomy in lymphocytes separates adaptive T and B lymphocytes, with clonally expressed antigen receptors, from innate lymphocytes, which carry out more rapid responses. Some T cell populations, however, are intermediates between these 2 poles, with the capacity to respond rapidly through T cell receptor activation or by cytokine stimulation. Here, using publicly available datasets, we constructed linear mixed models that not only define a gradient of innate gene expression in common for mouse innate-like T cells, but also are applicable to other mouse T lymphoid populations. A similar gradient could be identified for chromatin landscape based on ATAC-seq (assay for transposase-accessible chromatin using sequencing) data. The gradient included increased transcripts related to many traits of innate immune responses, with increased scores related to evidence for antigen experience. While including genes typical for T helper 1 (Th1) responses, the innateness gene program could be separated from Th1, Th2, and Th17 responses. Lymphocyte populations with higher innateness scores correlated with lower calcium-dependent T cell receptor-mediated cell activation, with some downstream signaling proteins dependent on calcium or affecting metabolism prephosphorylation. Therefore, as a group, different mouse innate-like T cell populations had related gene expression programs and activation pathways that are different from naive CD4 and CD8 T cells.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"214 2","pages":"223-237"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878997/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Rapid clonal expansion and somatic hypermutation contribute to the fate of SARS-CoV-2 broadly neutralizing antibodies. 快速克隆扩增和体细胞超突变有助于SARS-CoV-2广泛中和抗体的命运。

IF 3.6 3区医学

Journal of immunology Pub Date : 2025-02-01 DOI: 10.1093/jimmun/vkae056

Miao Wang, Congcong Liu, Qing Fan, Yuehong Sun, Shilong Tang, Huimin Guo, Bing Zhou, Haiyan Wang, Xiangyang Ge, Zheng Zhang, Bin Ju

{"title":"Rapid clonal expansion and somatic hypermutation contribute to the fate of SARS-CoV-2 broadly neutralizing antibodies.","authors":"Miao Wang, Congcong Liu, Qing Fan, Yuehong Sun, Shilong Tang, Huimin Guo, Bing Zhou, Haiyan Wang, Xiangyang Ge, Zheng Zhang, Bin Ju","doi":"10.1093/jimmun/vkae056","DOIUrl":"https://doi.org/10.1093/jimmun/vkae056","url":null,"abstract":"Several vaccines and immunization strategies, including inactivated vaccines, have proven effective in eliciting antibodies against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), providing an opportunity to characterize the antibody response. In this study, we investigated the monoclonal antibody responses elicited by wild-type SARS-CoV-2 inactivated vaccination compared to those elicited by natural infection and mRNA vaccination. The analysis showed that antibodies encoded by biased germline genes were shared between SARS-CoV-2 vaccinated and naturally infected individuals. Among the 35 shared clonotypes identified, besides the well-known IGHV3-53 and IGHV1-58, we identified a class of IGHV4-59 antibodies characterized by rapid response and neutralizing activity, elicited by 3 doses of inactivated vaccine. Members of this lineage exhibited similar sensitivity against wild-type SARS-CoV-2, whereas different neutralizing activities against SARS-CoV-2 variants, especially against various Omicron subvariants, BA.1, BA.2, BA.2.12.1, BA.4/5, and BA.2.75. Structural analysis of BA.1 spike complexed with VacBB-639 revealed that the IGHV4-59-lineage antibodies belonged to the Class 2/3 group. Using sequence alignment, site-mutation assays, and functional verification, we identified two substitutions, N60K in HFR3 and S56G in HCDR2, contributing to opposite neutralization changes of IGHV4-59-lineage antibodies against these Omicron subvariants. These results demonstrate the importance of somatic hypermutation in the evolution of prototypical antigen-elicited antibodies in terms of their neutralization breadth and potency against SARS-CoV-2 Omicron variants.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"214 2","pages":"278-289"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Ammonium chloride mitigates the amplification of fish virus by blocking autophagy-dependent replication. 氯化铵通过阻断依赖自噬的复制来减轻鱼病毒的扩增。

IF 3.6 3区医学

Journal of immunology Pub Date : 2025-02-01 DOI: 10.1093/jimmun/vkae012

Dan-Dan Chen, Jia-Xin Zhang, Zhuo-Cong Li, Can Zhang, Xiao Xu, Bao-Jie Cui, Na Xu, Yang-Yang Wang, Chu-Jing Zhou, Li Zhou, Long-Feng Lu, Shun Li

{"title":"Ammonium chloride mitigates the amplification of fish virus by blocking autophagy-dependent replication.","authors":"Dan-Dan Chen, Jia-Xin Zhang, Zhuo-Cong Li, Can Zhang, Xiao Xu, Bao-Jie Cui, Na Xu, Yang-Yang Wang, Chu-Jing Zhou, Li Zhou, Long-Feng Lu, Shun Li","doi":"10.1093/jimmun/vkae012","DOIUrl":"https://doi.org/10.1093/jimmun/vkae012","url":null,"abstract":"Ammonia fertilizer, primarily composed of ammonium chloride, is widely used in pond fish farming throughout Asia. Despite the belief that it possesses antiviral properties, the underlying mechanisms remain unclear. Ammonium chloride (NH4Cl) has been demonstrated to act as a potent inhibitor of autophagy, which is used by many fish viruses to promote their proliferation during infection. It was therefore hypothesized that the antiviral effect of ammonia fertilizers was likely due to the inhibition of autophagy in viruses. The present study sought to evaluate the antiviral effect of NH4Cl in a model of several fish cells and zebrafish. The findings demonstrated that the administration of NH4Cl after viral infection inhibited the proliferation of a variety of fish viruses, encompassing both DNA and RNA viruses. Further studies have indicated that NH4Cl obstructed autophagy-dependent virus proliferation of spring viremia of carp virus (SVCV) by inhibiting autophagic flux. The molecular mechanism revealed that SVCV contributed to the polyubiquitination of interferon regulatory factor 3 (IRF3) and promoted the degradation of IRF3 through cargo receptor sequestosome 1 (SQSTM1/p62)-mediated selective autophagy. However, NH4Cl was observed to inhibit SVCV-mediated selective autophagy of IRF3, thereby facilitating the production of interferon. Furthermore, the SVCV N protein was of critical importance in this process. Nevertheless, NH4Cl impeded this degradation process by inhibiting the autophagy pathway. The study found that NH4Cl was highly efficacious in controlling fish virus infection both in vivo and in vitro. It can therefore be concluded that the antiviral effect of ammonia fertilizers was, at least in part, due to the inhibition of viral autophagy.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"214 2","pages":"265-277"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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