European Journal of Immunology最新文献_第9页

Perioperative systemic IL-6 and immune-adipose- metabolism transcription in tumour and tumour adjacent breast cancer 肿瘤和肿瘤邻近乳腺癌围手术期全身 IL-6 和免疫-脂肪代谢转录。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-09-01 DOI: 10.1002/eji.202451049

Carolyn Cullinane, Roisin M. Connolly, Mark Corrigan, Henry P. Redmond, Cathriona Foley

{"title":"Perioperative systemic IL-6 and immune-adipose- metabolism transcription in tumour and tumour adjacent breast cancer","authors":"Carolyn Cullinane, Roisin M. Connolly, Mark Corrigan, Henry P. Redmond, Cathriona Foley","doi":"10.1002/eji.202451049","DOIUrl":"10.1002/eji.202451049","url":null,"abstract":"Surgical resection is the primary treatment approach for patients with breast cancer. Despite optimal multimodal treatment, metastatic recurrence remains a risk. Surgery-mediated systemic inflammation and local tissue inflammation generate an immunosuppressive and wound-healing environment that may accelerate cancer recurrence and metastasis post-operatively. Investigating the impact of surgery on local and systemic inflammation may provide knowledge for improvement of patient prognosis and treatment opportunities. Systemic cytokines were quantified in the blood plasma of patients with breast cancer pre-operatively, early post-operatively, and late post-operatively. Early post-operative levels of IL-6 were significantly elevated in patients who underwent mastectomy compared with wide local excision. Post-operative IL-6 levels correlate with clinicopathological features (age and BMI). The transcriptomes of local matched tumour and normal tumour adjacent (normal) breast tissue, from patients with breast cancer, were analysed by RNA-Seq. Elevated gene expressions of IL6, ADIPOQ, FABP4, LPL, PPARG, and CD36 in normal tissue were associated with worse overall survival of patients with ER-positive breast cancer. In tissue with higher expression of IL6 and ADIPOQ, a higher abundance of M2-like macrophage gene expression was identified. This study revealed perioperative systemic dynamics of inflammatory mediators and identified local immune-adipose-metabolism gene expression in tumour-adjacent tissue associated with pro-tumour function.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 11","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.202451049","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142102645","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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Lymphotoxins from distinct types of lymphoid cells differentially contribute to neuroinflammation 来自不同类型淋巴细胞的淋巴毒素对神经炎症的作用各不相同。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-08-29 DOI: 10.1002/eji.202350977

Violetta S. Gogoleva, Marina S. Drutskaya, Alexander I. Vorontsov, Kamar-Sulu N. Atretkhany, Alexey A. Belogurov Jr., Andrey A. Kruglov, Sergei A. Nedospasov

{"title":"Lymphotoxins from distinct types of lymphoid cells differentially contribute to neuroinflammation","authors":"Violetta S. Gogoleva, Marina S. Drutskaya, Alexander I. Vorontsov, Kamar-Sulu N. Atretkhany, Alexey A. Belogurov Jr., Andrey A. Kruglov, Sergei A. Nedospasov","doi":"10.1002/eji.202350977","DOIUrl":"10.1002/eji.202350977","url":null,"abstract":"Lymphotoxin α and lymphotoxin β (LTs), TNF superfamily members, are expressed in either soluble (LTα3) or membrane-bound (LTα1β2 or LTα2β1) forms. In the pathological context, LT-mediated signaling is known to exacerbate autoimmunity by perpetuating inflammation and promoting the formation of tertiary lymphoid organs. Despite this understanding, the exact roles of LTα and LTβ in the pathogenesis of the murine model of multiple sclerosis, and experimental autoimmune encephalomyelitis (EAE), remain controversial. Here, we employed a panel of gene-modified mice with cell-type restricted ablation of LTα (targeting both membrane-bound and soluble forms of LTs) to unravel the contributions of LTs from various lymphoid cells, namely T cells, type 3 innate lymphoid cells (ILC3) and B cells, in EAE. We found that the effects of LTα deletion were dependent on the cellular source. ILC3-derived lymphotoxins exerted a protective role in EAE by regulating the accumulation of IFN-ɣ- and GM-CSF-producing TH cells in the CNS. In contrast, T-cell-derived lymphotoxins promoted IL-17A- and GM-CSF-mediated TH responses in the periphery, whereas B-cell-derived lymphotoxins were pathogenic only in the autoantibody-mediated EAE model. Collectively, our findings unveil the multifaceted involvement of lymphotoxins in EAE pathogenesis and challenge the view that lymphotoxins play a solely pathogenic role in neuroinflammation.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 11","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142102644","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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Molecular and functional in vivo characterisation of murine Dectin-1 isoforms 小鼠 Dectin-1 异构体的分子和体内功能特征。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-08-28 DOI: 10.1002/eji.202451092

Nadja Leinung, Torben Mentrup, Sajma Hodzic, Bernd Schröder

{"title":"Molecular and functional in vivo characterisation of murine Dectin-1 isoforms","authors":"Nadja Leinung, Torben Mentrup, Sajma Hodzic, Bernd Schröder","doi":"10.1002/eji.202451092","DOIUrl":"10.1002/eji.202451092","url":null,"abstract":"Dectin-1 is a C-type lectin-receptor involved in sensing fungi by innate immune cells. Encoded by the Clec7a gene, Dectin-1 exists in two major splice isoforms, Dectin-1a and 1b, which differ in the presence of a membrane-proximal stalk domain. As reported previously, this domain determines degradative routes for Dectin-1a and 1b leading to the generation of a stable N-terminal fragment exclusively from Dectin-1a. Here, we narrow down the responsible part of the stalk and demonstrate the stabilisation of the Dectin-1a N-terminal fragment in tetraspanin-enriched microdomains. C57BL/6 and BALB/c mice show divergent Dectin-1 isoform expression patterns, which are caused by a single nucleotide polymorphism in exon 3 of the Clec7a gene, leading to a non-sense Dectin-1a mRNA in C57BL/6 mice. Using backcrossing, we generated mice with the C57BL/6 Clec7a allele on a BALB/c background and compared these to the parental strains. Expression of the C57BL/6 allele leads to the exclusive presence of the Dectin-1b protein. Furthermore, it was associated with higher Dectin-1 mRNA expression, but less Dectin-1 at the cell surface according to flow cytometry. In neutrophils, this altered ROS production induced by Dectin-1 model ligands, while cellular responses in macrophages and dendritic cells were not significantly influenced by the Dectin-1 isoform pattern.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 11","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.202451092","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142078542","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

Expansion of human γδ T cells in periphery: Lessons learned from development, infections, and compromised thymic function 人类γδ T 细胞在外周的扩增：从发育、感染和胸腺功能受损中汲取的教训。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-08-28 DOI: 10.1002/eji.202451073

Sarina Ravens, Eva Tolosa

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Expanding our understanding of Guillain–Barré syndrome: Recent advances and clinical implications 扩大我们对吉兰-巴雷综合征的认识：最新进展和临床意义。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-08-27 DOI: 10.1002/eji.202250336

Paolo Ripellino, Bettina Schreiner, Daniela Latorre

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The potential of γδ CAR and TRuC T cells: An unearthed treasure γδ CAR 和 TRuC T 细胞的潜力：出土的宝藏

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-08-27 DOI: 10.1002/eji.202451074

Wolfgang W. Schamel, Marina Zintchenko, Trang Nguyen, Boris Fehse, Priscilla S. Briquez, Susana Minguet

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The complement system: A key player in the host response to infections 补体系统：宿主应对感染的关键角色。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-08-27 DOI: 10.1002/eji.202350814

Archana Jayaraman, Sarah Walachowski, Markus Bosmann

{"title":"The complement system: A key player in the host response to infections","authors":"Archana Jayaraman, Sarah Walachowski, Markus Bosmann","doi":"10.1002/eji.202350814","DOIUrl":"10.1002/eji.202350814","url":null,"abstract":"Infections are one of the most significant healthcare and economic burdens across the world as underscored by the recent coronavirus pandemic. Moreover, with the increasing incidence of antimicrobial resistance, there is an urgent need to better understand host–pathogen interactions to design effective treatment strategies. The complement system is a key arsenal of the host defense response to pathogens and bridges both innate and adaptive immunity. However, in the contest between pathogens and host defense mechanisms, the host is not always victorious. Pathogens have evolved several approaches, including co-opting the host complement regulators to evade complement-mediated killing. Furthermore, deficiencies in the complement proteins, both genetic and therapeutic, can lead to an inefficient complement-mediated pathogen eradication, rendering the host more susceptible to certain infections. On the other hand, overwhelming infection can provoke fulminant complement activation with uncontrolled inflammation and potentially fatal tissue and organ damage. This review presents an overview of critical aspects of the complement-pathogen interactions during infection and discusses perspectives on designing therapies to mitigate complement dysfunction and limit tissue injury.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 11","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.202350814","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142071559","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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19th European Meeting on Complement in Human Diseases, September 2–6, 2024, Lübeck, Germany 特刊：第 19 届欧洲人类疾病补体会议，2024 年 9 月 2-6 日，德国吕贝克。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-08-22 DOI: 10.1002/eji.202470300

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Atg16l2 augments Nlrc4 inflammasome activation by facilitating NAIPs–NLRC4 association Atg16l2通过促进NAIPs-NLRC4的结合来增强Nlrc4炎性体的激活。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-08-22 DOI: 10.1002/eji.202451078

Zhoujin Wen, Tianli Yuan, Jiamin Liu, Dongyang Wang, Jun Ni, Xuehan Yan, Jian Tang, Jiayin Tang, Xuefeng Wu, Zheng Wang

{"title":"Atg16l2 augments Nlrc4 inflammasome activation by facilitating NAIPs–NLRC4 association","authors":"Zhoujin Wen, Tianli Yuan, Jiamin Liu, Dongyang Wang, Jun Ni, Xuehan Yan, Jian Tang, Jiayin Tang, Xuefeng Wu, Zheng Wang","doi":"10.1002/eji.202451078","DOIUrl":"10.1002/eji.202451078","url":null,"abstract":"As cytoplasmic protein complexes that are pivotal for innate immunity, inflammasomes act primarily through the detection of pathogen- or danger-associated molecular patterns. Nucleotide oligomerisation domain-like receptor family and caspase activation recruitment domain-containing protein 4 (NLRC4) inflammasomes identify and eliminate intracellular pathogens, a process contingent on the ligand-recognition capabilities of neuronal apoptosis inhibitory proteins (NAIPs). Upon detection of specific molecules indicative of intracellular infection, NAIPs discern distinct pathogenic components and subsequently transmit signals to NLRC4, thus initiating their activation and triggering an inflammatory response. However, the mechanisms underlying NLRC4 inflammasome remain unclear. In this study, we elucidated the critical role of ATG16L2 in activating the NLRC4 inflammasome. ATG16L2-deficient macrophages exhibited reduced NLRC4 inflammasome activation, characterised by decreased oligomerisation of apoptosis-associated speck-like protein containing a CARD and attenuated cleavage of Pro-caspase-1, Pro-IL-1β and gasdermin D. Co-immunoprecipitation assays revealed an interaction between ATG16L2 and NAIPs. Furthermore, ATG16L2 enhanced the association between NAIPs and NLRC4 by binding to NAIPs. For ATG16L2-knockout mice infected with Salmonella typhimurium, pathogen clearance and survival rates markedly decreased. Collectively, our findings suggest that ATG16L2 is a significant modulator of the innate immune system, influencing the activity of the NLRC4 inflammasome and the host's defensive response to intracellular pathogens.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 11","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.202451078","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142034661","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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7th European Conference of Immunology, 1–4 September, 2024, Dublin, Ireland 第 7 届欧洲免疫学会议，2024 年 9 月 1-4 日，爱尔兰都柏林

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-08-21 DOI: 10.1002/eji.202470200

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