Cellular &Molecular Immunology最新文献_第9页

Neuropilin-1high monocytes protect against neonatal inflammation 神经纤蛋白-1 高的单核细胞可防止新生儿发炎

IF 24.1 1区医学

Cellular &Molecular Immunology Pub Date : 2024-04-17 DOI: 10.1038/s41423-024-01157-7

Xiaoqing Zheng, Wen Lei, Yongmei Zhang, Han Jin, Cha Han, Fan Wu, Chonghong Jia, Ruihong Zeng, Zhanghua Chen, Yuxia Zhang, Haitao Wang, Qiang Liu, Zhi Yao, Ying Yu, Jie Zhou

{"title":"Neuropilin-1high monocytes protect against neonatal inflammation","authors":"Xiaoqing Zheng, Wen Lei, Yongmei Zhang, Han Jin, Cha Han, Fan Wu, Chonghong Jia, Ruihong Zeng, Zhanghua Chen, Yuxia Zhang, Haitao Wang, Qiang Liu, Zhi Yao, Ying Yu, Jie Zhou","doi":"10.1038/s41423-024-01157-7","DOIUrl":"10.1038/s41423-024-01157-7","url":null,"abstract":"Neonates are susceptible to inflammatory disorders such as necrotizing enterocolitis (NEC) due to their immature immune system. The timely appearance of regulatory immune cells in early life contributes to the control of inflammation in neonates, yet the underlying mechanisms of which remain poorly understood. In this study, we identified a subset of neonatal monocytes characterized by high levels of neuropilin-1 (Nrp1), termed Nrp1high monocytes. Compared with their Nrp1low counterparts, Nrp1high monocytes displayed potent immunosuppressive activity. Nrp1 deficiency in myeloid cells aggravated the severity of NEC, whereas adoptive transfer of Nrp1high monocytes led to remission of NEC. Mechanistic studies showed that Nrp1, by binding to its ligand Sema4a, induced intracellular p38-MAPK/mTOR signaling and activated the transcription factor KLF4. KLF4 transactivated Nos2 and enhanced the production of nitric oxide (NO), a key mediator of immunosuppression in monocytes. These findings reveal an important immunosuppressive axis in neonatal monocytes and provide a potential therapeutic strategy for treating inflammatory disorders in neonates.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"21 6","pages":"575-588"},"PeriodicalIF":24.1,"publicationDate":"2024-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140615913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Bypassing PELO-mediated ATPase activation of the NLR is a common pathogenic cause of NLR-associated autoinflammatory diseases 绕过 PELO 介导的 NLR ATPase 激活是 NLR 相关自身炎症性疾病的常见致病原因

IF 24.1 1区医学

Cellular &Molecular Immunology Pub Date : 2024-04-17 DOI: 10.1038/s41423-024-01162-w

Xiurong Wu, Zhang-Hua Yang, Yue Zheng, Jianfeng Wu, Jiahuai Han

引用次数: 0

Synthetic biology approaches for improving the specificity and efficacy of cancer immunotherapy 提高癌症免疫疗法特异性和疗效的合成生物学方法

IF 24.1 1区医学

Cellular &Molecular Immunology Pub Date : 2024-04-11 DOI: 10.1038/s41423-024-01153-x

Bo Zhu, Hang Yin, Di Zhang, Meiling Zhang, Xiaojuan Chao, Luca Scimeca, Ming-Ru Wu

{"title":"Synthetic biology approaches for improving the specificity and efficacy of cancer immunotherapy","authors":"Bo Zhu, Hang Yin, Di Zhang, Meiling Zhang, Xiaojuan Chao, Luca Scimeca, Ming-Ru Wu","doi":"10.1038/s41423-024-01153-x","DOIUrl":"10.1038/s41423-024-01153-x","url":null,"abstract":"Immunotherapy has shown robust efficacy in treating a broad spectrum of hematological and solid cancers. Despite the transformative impact of immunotherapy on cancer treatment, several outstanding challenges remain. These challenges include on-target off-tumor toxicity, systemic toxicity, and the complexity of achieving potent and sustainable therapeutic efficacy. Synthetic biology has emerged as a promising approach to overcome these obstacles, offering innovative tools for engineering living cells with customized functions. This review provides an overview of the current landscape and future prospects of cancer immunotherapy, particularly emphasizing the role of synthetic biology in augmenting its specificity, controllability, and efficacy. We delineate and discuss two principal synthetic biology strategies: those targeting tumor surface antigens with engineered immune cells and those detecting intratumoral disease signatures with engineered gene circuits. This review concludes with a forward-looking perspective on the enduring challenges in cancer immunotherapy and the potential breakthroughs that synthetic biology may contribute to the field.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"21 5","pages":"436-447"},"PeriodicalIF":24.1,"publicationDate":"2024-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41423-024-01153-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140581774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

GSNOR negatively regulates the NLRP3 inflammasome via S-nitrosation of MAPK14 GSNOR 通过 S-亚硝基化 MAPK14 负向调节 NLRP3 炎症体

IF 24.1 1区医学

Cellular &Molecular Immunology Pub Date : 2024-04-03 DOI: 10.1038/s41423-024-01155-9

Qianjin Liu, Lijin Jiao, Mao-Sen Ye, Zhiyu Ma, Jinsong Yu, Ling-Yan Su, Wei-Yin Zou, Lu-Xiu Yang, Chang Chen, Yong-Gang Yao

{"title":"GSNOR negatively regulates the NLRP3 inflammasome via S-nitrosation of MAPK14","authors":"Qianjin Liu, Lijin Jiao, Mao-Sen Ye, Zhiyu Ma, Jinsong Yu, Ling-Yan Su, Wei-Yin Zou, Lu-Xiu Yang, Chang Chen, Yong-Gang Yao","doi":"10.1038/s41423-024-01155-9","DOIUrl":"10.1038/s41423-024-01155-9","url":null,"abstract":"Hyperactivation of the NLRP3 inflammasome has been implicated in the pathogenesis of numerous diseases. However, the precise molecular mechanisms that modulate the transcriptional regulation of NLRP3 remain largely unknown. In this study, we demonstrated that S-nitrosoglutathione reductase (GSNOR) deficiency in macrophages leads to significant increases in the Nlrp3 and Il-1β expression levels and interleukin-1β (IL-1β) secretion in response to NLRP3 inflammasome stimulation. Furthermore, in vivo experiments utilizing Gsnor−/− mice revealed increased disease severity in both lipopolysaccharide (LPS)-induced septic shock and dextran sodium sulfate (DSS)-induced colitis models. Additionally, we showed that both LPS-induced septic shock and DSS-induced colitis were ameliorated in Gsnor−/− Nlrp3−/− double-knockout (DKO) mice. Mechanistically, GSNOR deficiency increases the S-nitrosation of mitogen-activated protein kinase 14 (MAPK14) at the Cys211 residue and augments MAPK14 kinase activity, thereby promoting Nlrp3 and Il-1β transcription and stimulating NLRP3 inflammasome activity. Our findings suggested that GSNOR is a regulator of the NLRP3 inflammasome and that reducing the level of S-nitrosylated MAPK14 may constitute an effective strategy for alleviating diseases associated with NLRP3-mediated inflammation.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"21 6","pages":"561-574"},"PeriodicalIF":24.1,"publicationDate":"2024-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140581781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Cellular metabolism regulates the differentiation and function of T-cell subsets 细胞代谢调节 T 细胞亚群的分化和功能

IF 24.1 1区医学

Cellular &Molecular Immunology Pub Date : 2024-04-02 DOI: 10.1038/s41423-024-01148-8

Sicong Ma, Yanan Ming, Jingxia Wu, Guoliang Cui

{"title":"Cellular metabolism regulates the differentiation and function of T-cell subsets","authors":"Sicong Ma, Yanan Ming, Jingxia Wu, Guoliang Cui","doi":"10.1038/s41423-024-01148-8","DOIUrl":"10.1038/s41423-024-01148-8","url":null,"abstract":"T cells are an important component of adaptive immunity and protect the host from infectious diseases and cancers. However, uncontrolled T cell immunity may cause autoimmune disorders. In both situations, antigen-specific T cells undergo clonal expansion upon the engagement and activation of antigens. Cellular metabolism is reprogrammed to meet the increase in bioenergetic and biosynthetic demands associated with effector T cell expansion. Metabolites not only serve as building blocks or energy sources to fuel cell growth and expansion but also regulate a broad spectrum of cellular signals that instruct the differentiation of multiple T cell subsets. The realm of immunometabolism research is undergoing swift advancements. Encapsulating all the recent progress within this concise review in not possible. Instead, our objective is to provide a succinct introduction to this swiftly progressing research, concentrating on the metabolic intricacies of three pivotal nutrient classes—lipids, glucose, and amino acids—in T cells. We shed light on recent investigations elucidating the roles of these three groups of metabolites in mediating the metabolic and immune functions of T cells. Moreover, we delve into the prospect of “editing” metabolic pathways within T cells using pharmacological or genetic approaches, with the aim of synergizing this approach with existing immunotherapies and enhancing the efficacy of antitumor and antiinfection immune responses.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"21 5","pages":"419-435"},"PeriodicalIF":24.1,"publicationDate":"2024-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41423-024-01148-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140602086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Defining two subpopulations of marginal zone B cells 定义边缘区 B 细胞的两个亚群

IF 24.1 1区医学

Cellular &Molecular Immunology Pub Date : 2024-03-27 DOI: 10.1038/s41423-024-01141-1

Xiaojing Liu, Fei-Long Meng

引用次数: 0

The chemerin-CMKLR1 axis in keratinocytes impairs innate host defense against cutaneous Staphylococcus aureus infection 角质细胞中的螯合素-CMKLR1轴会损害宿主对皮肤金黄色葡萄球菌感染的先天防御能力。

IF 24.1 1区医学

Cellular &Molecular Immunology Pub Date : 2024-03-26 DOI: 10.1038/s41423-024-01152-y

Yu Chen, Yan Song, Zhe Wang, Yangfan Lai, Wei Yin, Qian Cai, Miaomiao Han, Yiheng Cai, Yushan Xue, Zhengrong Chen, Xi Li, Jing Chen, Min Li, Huabin Li, Rui He

{"title":"The chemerin-CMKLR1 axis in keratinocytes impairs innate host defense against cutaneous Staphylococcus aureus infection","authors":"Yu Chen, Yan Song, Zhe Wang, Yangfan Lai, Wei Yin, Qian Cai, Miaomiao Han, Yiheng Cai, Yushan Xue, Zhengrong Chen, Xi Li, Jing Chen, Min Li, Huabin Li, Rui He","doi":"10.1038/s41423-024-01152-y","DOIUrl":"10.1038/s41423-024-01152-y","url":null,"abstract":"The skin is the most common site of Staphylococcus aureus infection, which can lead to various diseases, including invasive and life-threatening infections, through evasion of host defense. However, little is known about the host factors that facilitate the innate immune evasion of S. aureus in the skin. Chemerin, which is abundantly expressed in the skin and can be activated by proteases derived from S. aureus, has both direct bacteria-killing activity and immunomodulatory effects via interactions with its receptor CMKLR1. Here, we demonstrate that a lack of the chemerin/CMKLR1 axis increases the neutrophil-mediated host defense against S. aureus in a mouse model of cutaneous infection, whereas chemerin overexpression, which mimics high levels of chemerin in obese individuals, exacerbates S. aureus cutaneous infection. Mechanistically, we identified keratinocytes that express CMKLR1 as the main target of chemerin to suppress S. aureus-induced IL-33 expression, leading to impaired skin neutrophilia and bacterial clearance. CMKLR1 signaling specifically inhibits IL-33 expression induced by cell wall components but not secreted proteins of S. aureus by inhibiting Akt activation in mouse keratinocytes. Thus, our study revealed that the immunomodulatory effect of the chemerin/CMKLR1 axis mediates innate immune evasion of S. aureus in vivo and likely increases susceptibility to S. aureus infection in obese individuals.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"21 6","pages":"533-545"},"PeriodicalIF":24.1,"publicationDate":"2024-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140292909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Novel insights into regulation of butyrophilin molecules: critical components of cancer immunosurveillance by γδ T cells 丁嗜蛋白分子调控的新见解：γδ T 细胞对癌症免疫监视的关键成分。

IF 24.1 1区医学

Cellular &Molecular Immunology Pub Date : 2024-03-26 DOI: 10.1038/s41423-024-01138-w

Dieter Kabelitz

引用次数: 0

Aerobic glycolysis enables the effector differentiation potential of stem-like CD4+ T cells to combat cancer 有氧糖酵解使干性 CD4+ T 细胞具有抗癌的效应分化潜能。

IF 24.1 1区医学

Cellular &Molecular Immunology Pub Date : 2024-03-21 DOI: 10.1038/s41423-024-01154-w

Dawei Zou, Xiaolong Zhang, Shuang Li, Xiang Xiao, Nancy M. Gonzalez, Laurie J. Minze, Xian C. Li, Wenhao Chen

引用次数: 0

Insm1: orchestrating cellular mimicry in the thymus medulla Insm1：协调胸腺髓质中的细胞拟态

IF 24.1 1区医学

Cellular &Molecular Immunology Pub Date : 2024-03-19 DOI: 10.1038/s41423-024-01151-z

K. D. James, J. E. Cowan

引用次数: 0