Cellular &Molecular Immunology最新文献_第7页

Correction: Defining two subpopulations of marginal zone B cells 更正：边缘区 B 细胞两个亚群的定义。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2024-05-28 DOI: 10.1038/s41423-024-01175-5

Xiaojing Liu, Fei-Long Meng

引用次数: 0

The protective roles of integrin α4β7 and Amphiregulin-expressing innate lymphoid cells in lupus nephritis 狼疮肾炎中整合素α4β7和Amphiregulin表达的先天淋巴细胞的保护作用。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2024-05-28 DOI: 10.1038/s41423-024-01178-2

Seungwon Ryu, Kyung Ah Kim, Jinwoo Kim, Dong Hun Lee, Yong-Soo Bae, Hajeong Lee, Byoung Choul Kim, Hye Young Kim

{"title":"The protective roles of integrin α4β7 and Amphiregulin-expressing innate lymphoid cells in lupus nephritis","authors":"Seungwon Ryu, Kyung Ah Kim, Jinwoo Kim, Dong Hun Lee, Yong-Soo Bae, Hajeong Lee, Byoung Choul Kim, Hye Young Kim","doi":"10.1038/s41423-024-01178-2","DOIUrl":"10.1038/s41423-024-01178-2","url":null,"abstract":"Type 2 innate lymphoid cells (ILC2s) have emerged as key regulators of the immune response in renal inflammatory diseases such as lupus nephritis. However, the mechanisms underlying ILC2 adhesion and migration in the kidney remain poorly understood. Here, we revealed the critical role of integrin α4β7 in mediating renal ILC2 adhesion and function. We found that integrin α4β7 enables the retention of ILC2s in the kidney by binding to VCAM-1, E-cadherin, or fibronectin on structural cells. Moreover, integrin α4β7 knockdown reduced the production of the reparative cytokine amphiregulin (Areg) by ILC2s. In lupus nephritis, TLR7/9 signaling within the kidney microenvironment downregulates integrin α4β7 expression, leading to decreased Areg production and promoting the egress of ILC2s. Notably, IL-33 treatment upregulated integrin α4β7 and Areg expression in ILC2s, thereby enhancing survival and reducing inflammation in lupus nephritis. Together, these findings highlight the potential of targeting ILC2 adhesion as a therapeutic strategy for autoimmune kidney diseases.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"21 7","pages":"723-737"},"PeriodicalIF":21.8,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11214630/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141160848","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

Targeting STING in dendritic cells alleviates psoriatic inflammation by suppressing IL-17A production 靶向树突状细胞中的 STING 可抑制 IL-17A 的产生，从而缓解银屑病炎症。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2024-05-28 DOI: 10.1038/s41423-024-01160-y

Xiaoying Sun, Liu Liu, Jiao Wang, Xiaorong Luo, Meng Wang, Chunxiao Wang, Jiale Chen, Yaqiong Zhou, Hang Yin, Yuanbin Song, Yuanyan Xiong, Hongjin Li, Meiling Zhang, Bo Zhu, Xin Li

{"title":"Targeting STING in dendritic cells alleviates psoriatic inflammation by suppressing IL-17A production","authors":"Xiaoying Sun, Liu Liu, Jiao Wang, Xiaorong Luo, Meng Wang, Chunxiao Wang, Jiale Chen, Yaqiong Zhou, Hang Yin, Yuanbin Song, Yuanyan Xiong, Hongjin Li, Meiling Zhang, Bo Zhu, Xin Li","doi":"10.1038/s41423-024-01160-y","DOIUrl":"10.1038/s41423-024-01160-y","url":null,"abstract":"Psoriasis is a common chronic inflammatory skin disease driven by the aberrant activation of dendritic cells (DCs) and T cells, ultimately leading to increased production of cytokines such as interleukin (IL)-23 and IL-17A. It is established that the cGAS-STING pathway is essential for psoriatic inflammation, however, the specific role of cGAS-STING signaling in DCs within this context remains unclear. In this study, we demonstrated the upregulation of cGAS-STING signaling in psoriatic lesions by analyzing samples from both clinical patients and imiquimod (IMQ)-treated mice. Using a conditional Sting-knockout transgenic mouse model, we elucidated the impact of cGAS-STING signaling in DCs on the activation of IL-17- and IFN-γ-producing T cells in psoriatic inflammation. Ablation of the Sting hampers DC activation leads to decreased numbers of IL-17-producing T cells and Th1 cells, and thus subsequently attenuates psoriatic inflammation in the IMQ-induced mouse model. Furthermore, we explored the therapeutic potential of the STING inhibitor C-176, which reduces psoriatic inflammation and enhances the anti-IL-17A therapeutic response. Our results underscore the critical role of cGAS-STING signaling in DCs in driving psoriatic inflammation and highlight a promising psoriasis treatment.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"21 7","pages":"738-751"},"PeriodicalIF":21.8,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141160893","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

Bridging the gap with multispecific immune cell engagers in cancer and infectious diseases 利用多特异性免疫细胞参与剂弥合癌症和传染病领域的差距。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2024-05-24 DOI: 10.1038/s41423-024-01176-4

Camille Rolin, Jacques Zimmer, Carole Seguin-Devaux

{"title":"Bridging the gap with multispecific immune cell engagers in cancer and infectious diseases","authors":"Camille Rolin, Jacques Zimmer, Carole Seguin-Devaux","doi":"10.1038/s41423-024-01176-4","DOIUrl":"10.1038/s41423-024-01176-4","url":null,"abstract":"By binding to multiple antigens simultaneously, multispecific antibodies are expected to substantially improve both the activity and long-term efficacy of antibody-based immunotherapy. Immune cell engagers, a subclass of antibody-based constructs, consist of engineered structures designed to bridge immune effector cells to their target, thereby redirecting the immune response toward the tumor cells or infected cells. The increasing number of recent clinical trials evaluating immune cell engagers reflects the important role of these molecules in new therapeutic approaches for cancer and infections. In this review, we discuss how different immune cell types (T and natural killer lymphocytes, as well as myeloid cells) can be bound by immune cell engagers in immunotherapy for cancer and infectious diseases. Furthermore, we explore the preclinical and clinical advancements of these constructs, and we discuss the challenges in translating the current knowledge from cancer to the virology field. Finally, we speculate on the promising future directions that immune cell engagers may take in cancer treatment and antiviral therapy.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"21 7","pages":"643-661"},"PeriodicalIF":21.8,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11214628/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141092312","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

Neutrophils disrupt B-1a cell homeostasis by targeting Siglec-G to exacerbate sepsis 中性粒细胞通过靶向 Siglec-G 破坏 B-1a 细胞稳态，从而加剧败血症。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2024-05-24 DOI: 10.1038/s41423-024-01165-7

Chuyi Tan, Bridgette Reilly, Gaifeng Ma, Atsushi Murao, Alok Jha, Monowar Aziz, Ping Wang

{"title":"Neutrophils disrupt B-1a cell homeostasis by targeting Siglec-G to exacerbate sepsis","authors":"Chuyi Tan, Bridgette Reilly, Gaifeng Ma, Atsushi Murao, Alok Jha, Monowar Aziz, Ping Wang","doi":"10.1038/s41423-024-01165-7","DOIUrl":"10.1038/s41423-024-01165-7","url":null,"abstract":"B-1a cells, an innate-like cell population, are crucial for pathogen defense and the regulation of inflammation through their release of natural IgM and IL-10. In sepsis, B-1a cell numbers are decreased in the peritoneal cavity as they robustly migrate to the spleen. Within the spleen, migrating B-1a cells differentiate into plasma cells, leading to alterations in their original phenotype and functionality. We discovered a key player, sialic acid-binding immunoglobulin-like lectin-G (Siglec-G), which is expressed predominantly on B-1a cells and negatively regulates B-1a cell migration to maintain homeostasis. Siglec-G interacts with CXCR4/CXCL12 to modulate B-1a cell migration. Neutrophils aid B-1a cell migration via neutrophil elastase (NE)-mediated Siglec-G cleavage. Human studies revealed increased NE expression in septic patients. We identified an NE cleavage sequence in silico, leading to the discovery of a decoy peptide that protects Siglec-G, preserves peritoneal B-1a cells, reduces inflammation, and enhances sepsis survival. The role of Siglec-G in inhibiting B-1a cell migration to maintain their inherent phenotype and function is compromised by NE in sepsis, offering valuable insights into B-1a cell homeostasis. Employing a small decoy peptide to prevent NE-mediated Siglec-G cleavage has emerged as a promising strategy to sustain peritoneal B-1a cell homeostasis, alleviate inflammation, and ultimately improve outcomes in sepsis patients.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"21 7","pages":"707-722"},"PeriodicalIF":21.8,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141092447","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

The role of plasmacytoid dendritic cells (pDCs) in immunity during viral infections and beyond 质体树突状细胞（pDCs）在病毒感染期间及以后的免疫中的作用。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2024-05-22 DOI: 10.1038/s41423-024-01167-5

Clémence Ngo, Clémence Garrec, Elena Tomasello, Marc Dalod

{"title":"The role of plasmacytoid dendritic cells (pDCs) in immunity during viral infections and beyond","authors":"Clémence Ngo, Clémence Garrec, Elena Tomasello, Marc Dalod","doi":"10.1038/s41423-024-01167-5","DOIUrl":"10.1038/s41423-024-01167-5","url":null,"abstract":"Type I and III interferons (IFNs) are essential for antiviral immunity and act through two different but complimentary pathways. First, IFNs activate intracellular antimicrobial programs by triggering the upregulation of a broad repertoire of viral restriction factors. Second, IFNs activate innate and adaptive immunity. Dysregulation of IFN production can lead to severe immune system dysfunction. It is thus crucial to identify and characterize the cellular sources of IFNs, their effects, and their regulation to promote their beneficial effects and limit their detrimental effects, which can depend on the nature of the infected or diseased tissues, as we will discuss. Plasmacytoid dendritic cells (pDCs) can produce large amounts of all IFN subtypes during viral infection. pDCs are resistant to infection by many different viruses, thus inhibiting the immune evasion mechanisms of viruses that target IFN production or their downstream responses. Therefore, pDCs are considered essential for the control of viral infections and the establishment of protective immunity. A thorough bibliographical survey showed that, in most viral infections, despite being major IFN producers, pDCs are actually dispensable for host resistance, which is achieved by multiple IFN sources depending on the tissue. Moreover, primary innate and adaptive antiviral immune responses are only transiently affected in the absence of pDCs. More surprisingly, pDCs and their IFNs can be detrimental in some viral infections or autoimmune diseases. This makes the conservation of pDCs during vertebrate evolution an enigma and thus raises outstanding questions about their role not only in viral infections but also in other diseases and under physiological conditions.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"21 9","pages":"1008-1035"},"PeriodicalIF":21.8,"publicationDate":"2024-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41423-024-01167-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141079742","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

Liver kinase B1 (LKB1) staves off γδ T-cell-mediated autoimmune liver disease 肝激酶 B1 (LKB1) 阻止了 γδ T 细胞介导的自身免疫性肝病。

IF 24.1 1区医学

Cellular &Molecular Immunology Pub Date : 2024-05-16 DOI: 10.1038/s41423-024-01172-8

Yiwen Wang, Lan Wu, Luc Van Kaer

引用次数: 0

Chemerin is a key player in antimicrobial defense in skin 螯合素是皮肤抗菌防御的关键因素。

IF 24.1 1区医学

Cellular &Molecular Immunology Pub Date : 2024-05-16 DOI: 10.1038/s41423-024-01159-5

Silvano Sozzani, Francesca Sozio, Annalisa Del Prete

引用次数: 0

Neutrophil–macrophage communication via extracellular vesicle transfer promotes itaconate accumulation and ameliorates cytokine storm syndrome 中性粒细胞-巨噬细胞通过细胞外囊泡转移进行交流，促进了伊塔康酸的积累并改善了细胞因子风暴综合征。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2024-05-14 DOI: 10.1038/s41423-024-01174-6

Haixia Kang, Ting Liu, Yuanyuan Wang, Wenjuan Bai, Yan Luo, Jing Wang

{"title":"Neutrophil–macrophage communication via extracellular vesicle transfer promotes itaconate accumulation and ameliorates cytokine storm syndrome","authors":"Haixia Kang, Ting Liu, Yuanyuan Wang, Wenjuan Bai, Yan Luo, Jing Wang","doi":"10.1038/s41423-024-01174-6","DOIUrl":"10.1038/s41423-024-01174-6","url":null,"abstract":"Cytokine storm syndrome (CSS) is a life-threatening systemic inflammatory syndrome involving innate immune hyperactivity triggered by various therapies, infections, and autoimmune conditions. However, the potential interplay between innate immune cells is not fully understood. Here, using poly I:C and lipopolysaccharide (LPS)-induced cytokine storm models, a protective role of neutrophils through the modulation of macrophage activation was identified in a CSS model. Intravital imaging revealed neutrophil-derived extracellular vesicles (NDEVs) in the liver and spleen, which were captured by macrophages. NDEVs suppressed proinflammatory cytokine production by macrophages when cocultured in vitro or infused into CSS models. Metabolic profiling of macrophages treated with NDEV revealed elevated levels of the anti-inflammatory metabolite, itaconate, which is produced from cis-aconitate in the Krebs cycle by cis-aconitate decarboxylase (Acod1, encoded by Irg1). Irg1 in macrophages, but not in neutrophils, was critical for the NDEV-mediated anti-inflammatory effects. Mechanistically, NDEVs delivered miR-27a-3p, which suppressed the expression of Suclg1, the gene encoding the enzyme that metabolizes itaconate, thereby resulting in the accumulation of itaconate in macrophages. These findings demonstrated that neutrophil-to-macrophage communication mediated by extracellular vesicles is critical for promoting the anti-inflammatory reprogramming of macrophages in CSS and may have potential implications for the treatment of this fatal condition.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"21 7","pages":"689-706"},"PeriodicalIF":21.8,"publicationDate":"2024-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140921447","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 the sexual dimorphism-associated immune response 对性双态相关免疫反应的新认识。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2024-05-13 DOI: 10.1038/s41423-024-01177-3

José M. Izquierdo

引用次数: 0