European Journal of Immunology最新文献_第6页

Bridging the gap: Insights in the immunopathology of Lyme borreliosis 缩小差距：莱姆包虫病免疫病理学的启示。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-10-13 DOI: 10.1002/eji.202451063

Marijn E. Snik, Noor E.I.M. Stouthamer, Joppe W. Hovius, Melissa M.J. van Gool

{"title":"Bridging the gap: Insights in the immunopathology of Lyme borreliosis","authors":"Marijn E. Snik, Noor E.I.M. Stouthamer, Joppe W. Hovius, Melissa M.J. van Gool","doi":"10.1002/eji.202451063","DOIUrl":"10.1002/eji.202451063","url":null,"abstract":"Lyme borreliosis (LB), caused by Borrelia burgdorferi sensu lato (Bbsl) genospecies transmitted by Ixodes spp. ticks, is a significant public health concern in the Northern Hemisphere. This review highlights the complex interplay between Bbsl infection and host–immune responses, impacting clinical manifestations and long-term immunity. Early localized disease is characterized by erythema migrans (EM), driven by T-helper 1 (Th1) responses and proinflammatory cytokines. Dissemination to the heart and CNS can lead to Lyme carditis and neuroborreliosis respectively, orchestrated by immune cell infiltration and chemokine dysregulation. More chronic manifestations, including acrodermatitis chronica atrophicans and Lyme arthritis, involve prolonged inflammation as well as the development of autoimmunity. In addition, dysregulated immune responses impair long-term immunity, with compromised B-cell memory and antibody responses. Experimental models and clinical studies underscore the role of Th1/Th2 balance, B-cell dysfunction, and autoimmunity in LB pathogenesis. Moreover, LB-associated autoimmunity parallels mechanisms observed in other infectious and autoimmune diseases. Understanding immune dysregulation in LB provides insights into disease heterogeneity and could provide new strategies for diagnosis and treatment.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628917/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142454216","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}

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Cover Story: Eur. J. Immunol. 10'24 封面故事Eur.J. Immunol.10'24

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-10-04 DOI: 10.1002/eji.202470101

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Highly sensitive reporter cell line for detection of interferon types I–III and their neutralization by antibodies 用于检测 I-III 型干扰素及其抗体中和的高灵敏报告细胞系。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-10-04 DOI: 10.1002/eji.202451325

Kevin Groen, Roger Kuratli, Lauren Sar, Andri Vasou, Michael Huber, David J. Hughes, Benjamin G. Hale

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Impressum 印象深刻。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-10-04 DOI: 10.1002/eji.202470103

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Issue Information: Eur. J. Immunol. 10'24 发行信息：Eur.J. Immunol.10'24

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-10-04 DOI: 10.1002/eji.202470102

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A20 intrinsically influences human effector T-cell survival and function by regulating both NF-κB and JNK signaling A20 通过调节 NF-κB 和 JNK 信号，从本质上影响人类效应 T 细胞的存活和功能。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-10-02 DOI: 10.1002/eji.202451245

Gina Dabbah-Krancher, Allison Ruchinskas, Melissa A. Kallarakal, Katherine P. Lee, Bradly M. Bauman, Benjamin Epstein, Hongli Yin, Daniel Krappmann, Brian C. Schaefer, Andrew L. Snow

{"title":"A20 intrinsically influences human effector T-cell survival and function by regulating both NF-κB and JNK signaling","authors":"Gina Dabbah-Krancher, Allison Ruchinskas, Melissa A. Kallarakal, Katherine P. Lee, Bradly M. Bauman, Benjamin Epstein, Hongli Yin, Daniel Krappmann, Brian C. Schaefer, Andrew L. Snow","doi":"10.1002/eji.202451245","DOIUrl":"10.1002/eji.202451245","url":null,"abstract":"A20 is a dual-function ubiquitin-editing enzyme that maintains immune homeostasis by restraining inflammation. Although A20 serves a similar negative feedback function for T-cell receptor (TCR) signaling, the molecular mechanisms utilized and their ultimate impact on human T-cell function remain unclear. TCR engagement triggers the assembly of the CARD11-BCL10-MALT1 (CBM) protein complex, a signaling platform that governs the activation of downstream transcription factors including NF-κB and c-Jun/AP-1. Utilizing WT and A20 knockout Jurkat T cells, we found that A20 is required to negatively regulate NF-κB and JNK. Utilizing a novel set of A20 mutants in NF-κB and AP-1-driven reporter systems, we discovered the ZnF7 domain is crucial for negative regulatory capacity, while deubiquitinase activity is dispensable. Successful inactivation of A20 in human primary effector T cells congruently conferred sustained NF-κB and JNK signaling, including enhanced upregulation of activation markers, and increased secretion of several cytokines including IL-9. Finally, loss of A20 in primary human T cells resulted in decreased sensitivity to restimulation-induced cell death and increased sensitivity to cytokine withdrawal-induced death. These findings demonstrate the importance of A20 in maintaining T-cell homeostasis via negative regulation of both NF-κB and JNK signaling.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142363607","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}

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Chronic stimulation desensitizes β2-adrenergic receptor responses in natural killer cells 慢性刺激可使自然杀伤细胞中的β2-肾上腺素能受体反应脱敏。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-09-30 DOI: 10.1002/eji.202451299

Martin Jürgens, Maren Claus, Sabine Wingert, Jens Alexander Niemann, Lea Katharina Picard, Elisabeth Hennes, Ina Haasler, Birte Hellwig, Nina Overbeck, Jörg Reinders, Jörg Rahnenführer, Michaela Schedel, Silvia Capellino, Carsten Watzl

{"title":"Chronic stimulation desensitizes β2-adrenergic receptor responses in natural killer cells","authors":"Martin Jürgens, Maren Claus, Sabine Wingert, Jens Alexander Niemann, Lea Katharina Picard, Elisabeth Hennes, Ina Haasler, Birte Hellwig, Nina Overbeck, Jörg Reinders, Jörg Rahnenführer, Michaela Schedel, Silvia Capellino, Carsten Watzl","doi":"10.1002/eji.202451299","DOIUrl":"10.1002/eji.202451299","url":null,"abstract":"Adrenergic receptors (ARs) are preferentially expressed by innate lymphocytes such as natural killer (NK) cells. Here, we study the effect of epinephrine-mediated stimulation of the β2-adrenergic receptor (β2AR) on the function of human NK cells. Epinephrine stimulation inhibited early NK cell signaling events and blocked the function of the integrin LFA-1. This reduced the adhesion of NK cells to ICAM-1, explaining how NK cells are mobilized into the peripheral blood upon epinephrine release during acute stress or exercise. Additionally, epinephrine stimulation transiently reduced NK cell degranulation, serial killing, and cytokine production and affected metabolic changes upon NK cell activation via the cAMP-protein kinase A (PKA) pathway. Repeated exposure to β2AR agonists resulted in the desensitization of the β2AR via a PKA feedback loop-initiated G-protein switch. Therefore, acute epinephrine stimulation of chronically β2AR stimulated NK cells no longer resulted in inhibited signaling and reduced LFA-1 activity. Sustained stimulation by long-acting β2-agonists (LABA) not only inhibited NK cell functions but also resulted in desensitization of the β2AR. However, peripheral NK cells from LABA-treated asthma patients still reacted unchanged to epinephrine stimulation, demonstrating that local LABA administration does not result in detectable systemic effects on NK cells.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628883/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142337930","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

Liver type 1 innate lymphoid cells undergo apoptosis in murine models of macrophage activation syndrome and are dispensable for disease 在巨噬细胞活化综合征小鼠模型中，肝脏1型先天性淋巴细胞会发生凋亡，对疾病来说是不可或缺的。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-09-30 DOI: 10.1002/eji.202451043

Amber De Visscher, Marte Vandeput, Jessica Vandenhaute, Bert Malengier-Devlies, Eline Bernaerts, Kourosh Ahmadzadeh, Jessica Filtjens, Tania Mitera, Nele Berghmans, Philippe E. Van den Steen, Christin Friedrich, Georg Gasteiger, Carine Wouters, Patrick Matthys

{"title":"Liver type 1 innate lymphoid cells undergo apoptosis in murine models of macrophage activation syndrome and are dispensable for disease","authors":"Amber De Visscher, Marte Vandeput, Jessica Vandenhaute, Bert Malengier-Devlies, Eline Bernaerts, Kourosh Ahmadzadeh, Jessica Filtjens, Tania Mitera, Nele Berghmans, Philippe E. Van den Steen, Christin Friedrich, Georg Gasteiger, Carine Wouters, Patrick Matthys","doi":"10.1002/eji.202451043","DOIUrl":"10.1002/eji.202451043","url":null,"abstract":"Macrophage activation syndrome (MAS) exemplifies a severe cytokine storm disorder with liver inflammation. In the liver, classical natural killer (cNK) cells and liver-resident type 1 innate lymphoid cells (ILC1s) dominate the ILC population. Thus far, research has primarily focused on the corresponding role of cNK cells. Considering the liver inflammation and cytokine storm in MAS, liver-resident ILC1s represent an interesting population to explore due to their rapid cytokine production upon environmental triggers. By utilizing a Toll-like receptor (TLR)9- and TLR3:4-triggered MAS model, we showed that ILC1s highly produce IFN-γ and TNF-α. However, activated ILC1s undergo apoptosis and are strongly reduced in numbers, while cNK cells resist inflammation-induced apoptosis. Signs of mitochondrial stress suggest that this ILC1 apoptosis may be driven by inflammation-induced mitochondrial impairment. To study whether early induction of highly cytokine-producing ILC1s influences MAS development, we used Hobit KO mice due to their paucity of liver ILC1s but unaffected cNK cell numbers. Nevertheless, neither the severity of MAS features nor the total inflammatory cytokine levels were affected in these Hobit KO mice, indicating that ILC1s are dispensable for MAS pathogenesis. Collectively, our data demonstrate that ILC1s undergo apoptosis during TLR-triggering and are dispensable for MAS pathogenesis.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142337931","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}

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Sphingosine-1-phosphate receptor type 4 is critically involved in the regulation of peritoneal B-1 cell trafficking and distribution in vivo 鞘氨醇-1-磷酸受体4型在体内参与调节腹膜B-1细胞的贩运和分布。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-09-29 DOI: 10.1002/eji.202350882

Janik Riese, Annabel Kleinwort, Maurice Hannemann, Celine Hähnel, Stephan Kersting, Tobias Schulze

{"title":"Sphingosine-1-phosphate receptor type 4 is critically involved in the regulation of peritoneal B-1 cell trafficking and distribution in vivo","authors":"Janik Riese, Annabel Kleinwort, Maurice Hannemann, Celine Hähnel, Stephan Kersting, Tobias Schulze","doi":"10.1002/eji.202350882","DOIUrl":"10.1002/eji.202350882","url":null,"abstract":"B-1 cells are crucially involved in immune defense and regulation of inflammation and autoimmunity. B-1 cells are predominantly located in the peritoneal and pleural cavities, although body cavity B-1 cells recirculate systemically under steady-state conditions. The chemokines CXCL12 and CXCL13 have been identified as the main regulators of peritoneal B-cell trafficking. In mice deficient for sphingosine-1-phosphate receptor 4 (S1PR4), B-1a and B-1b cell numbers are reduced in the peritoneal cavity by an unknown mechanism. In this study, we show that S1PR4-mediated S1P signaling modifies the chemotactic response of peritoneal B cells to CXCL13 and CXCL12 in vitro. In vivo, S1PR4-mediated S1P signaling affects both immigration into and emigration from the peritoneal cavity. Long-term reconstitution experiments of scid mice with wt or s1pr4–/– peritoneal B cells revealed a distinct distributional pattern in secondary lymphoid organs. As a functional consequence, both plasmatic and mucosal IgM levels, the main product of B-1a cells, are reduced in mice reconstituted with s1pr4–/– peritoneal cells. In summary, our data identify S1PR4 as the second S1P receptor (besides S1PR1), which is critically involved in the regulation of peritoneal B-1 cell function.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628879/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142337932","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}

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Innate immunity champions: The diverse functions of macrophages 先天免疫冠军：巨噬细胞的多种功能

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-09-23 DOI: 10.1002/eji.202451139

Francesca Biscu, Anissa Zouzaf, Donatella Cicia, Clare Pridans, Gianluca Matteoli

{"title":"Innate immunity champions: The diverse functions of macrophages","authors":"Francesca Biscu, Anissa Zouzaf, Donatella Cicia, Clare Pridans, Gianluca Matteoli","doi":"10.1002/eji.202451139","DOIUrl":"10.1002/eji.202451139","url":null,"abstract":"Macrophages are instrumental in maintaining tissue homeostasis, modulating inflammation, and driving regeneration. The advent of omics techniques has led to the identification of numerous tissue-specific macrophage subtypes, thereby introducing the concept of the “macrophage niche”. This paradigm underscores the ability of macrophages to adapt their functions based on environmental cues, such as tissue-specific signals. This adaptability is closely linked to their metabolic states, which are crucial for their function and role in health and disease. Macrophage metabolism is central to their ability to switch between proinflammatory and anti-inflammatory states. In this regard, environmental factors, including the extracellular matrix, cellular interactions, and microbial metabolites, profoundly influence macrophage behavior. Moreover, diet and gut microbiota significantly impact macrophage function, with nutrients and microbial metabolites influencing their activity and contributing to conditions like inflammatory bowel disease. Targeting specific macrophage functions and their metabolic processes is leading to the development of novel treatments for a range of chronic inflammatory conditions. The exploration of macrophage biology enriches our understanding of immune regulation and holds the promise of innovative approaches to managing diseases marked by inflammation and immune dysfunction, offering a frontier for scientific and clinical advancement.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.202451139","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142277634","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