European Journal of Immunology最新文献_第8页

Bead-by-bead normalization of single antigen assays: A necessary step for accurate detection of weak anti-HLA antibodies 单抗原检测的逐珠归一化：准确检测弱抗 HLA 抗体的必要步骤。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-09-05 DOI: 10.1002/eji.202451181

Cédric Usureau, Romain Lhotte, Magali Devriese, Jérémy Siemowski, Lionel Gabet, Véronique Letort, Jean-Luc Taupin

{"title":"Bead-by-bead normalization of single antigen assays: A necessary step for accurate detection of weak anti-HLA antibodies","authors":"Cédric Usureau, Romain Lhotte, Magali Devriese, Jérémy Siemowski, Lionel Gabet, Véronique Letort, Jean-Luc Taupin","doi":"10.1002/eji.202451181","DOIUrl":"10.1002/eji.202451181","url":null,"abstract":"Ascertaining the presence of weakly positive anti-HLA donor-specific antibodies (DSA) in organ transplantation with multiplex single antigen beads assays may be challenging despite their high sensitivity due to technical variability issues. Through extensive datasets of Next-Generation Sequencing HLA typings and single antigen analyses, we reassessed the mean fluorescence intensity (MFI) positivity threshold of the assay to enhance accuracy. By showing that some beads were more prone to false positivity than others, we propose a nuanced approach that accounts for nonspecific intrinsic reactivities at the HLA antigen level, that is, on a bead-by-bead basis, as it enhances assay precision and reliability. This is substantiated by a comprehensive statistical analysis of MFI values and the implementation of the determination of a “Quantile Adjusted Threshold 500” (QAT500) value for each bead. Applied to DSA detection during patients’ follow-up, this approach discriminated better and earlier low-strength DSA that would later raise their MFI above the clinically relevant threshold of 3000. Moving from a subjective interpretation to a more objective and precise methodology allows for standardizing HLA antibody and DSA detection. The study emphasizes the need for further research with real clinical data to validate and refine this approach.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 11","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.202451181","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131317","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

Tviblindi algorithm identifies branching developmental trajectories of human B-cell development and describes abnormalities in RAG-1 and WAS patients Tviblindi 算法识别了人类 B 细胞发育的分支发育轨迹，并描述了 RAG-1 和 WAS 患者的异常情况。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-09-05 DOI: 10.1002/eji.202451004

Marina Bakardjieva, Ondřej Pelák, Marjolein Wentink, Hana Glier, David Novák, Jitka Stančíková, Daniela Kužílková, Ester Mejstříková, Iga Janowska, Marta Rizzi, Mirjam van der Burg, Jan Stuchlý, Tomáš Kalina

{"title":"Tviblindi algorithm identifies branching developmental trajectories of human B-cell development and describes abnormalities in RAG-1 and WAS patients","authors":"Marina Bakardjieva, Ondřej Pelák, Marjolein Wentink, Hana Glier, David Novák, Jitka Stančíková, Daniela Kužílková, Ester Mejstříková, Iga Janowska, Marta Rizzi, Mirjam van der Burg, Jan Stuchlý, Tomáš Kalina","doi":"10.1002/eji.202451004","DOIUrl":"10.1002/eji.202451004","url":null,"abstract":"Detailed knowledge of human B-cell development is crucial for the proper interpretation of inborn errors of immunity and malignant diseases. It is of interest to understand the kinetics of protein expression changes during development, but also to properly interpret the major and possibly alternative developmental trajectories. We have investigated human samples from healthy individuals with the aim of describing all B-cell developmental trajectories. We validated a 30-parameter mass cytometry panel and demonstrated the utility of “vaevictis” visualization of B-cell developmental stages. We used the trajectory inference tool “tviblindi” to exhaustively describe all trajectories leading to all developmental ends discovered in the data. Focusing on Natural Effector B cells, we demonstrated the dynamics of expression of nuclear factors (PAX-5, TdT, Ki-67, Bcl-2), cytokine and chemokine receptors (CD127, CXCR4, CXCR5) in relation to the canonical B-cell developmental stage markers. We observed branching of the memory development, where follicular memory formation was marked by CD73 expression. Lastly, we performed an analysis of two example cases of abnormal B-cell development caused by mutations in RAG-1 and Wiskott–Aldrich syndrome gene in patients with primary immunodeficiency. In conclusion, we developed, validated, and presented a comprehensive set of tools for the investigation of B-cell development in the bone marrow compartment.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628918/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131388","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

Innate T-cell-derived IL-17A/F protects from bleomycin-induced acute lung injury but not bleomycin or adenoviral TGF-β1-induced lung fibrosis in mice 先天性 T 细胞衍生的 IL-17A/F 可保护小鼠免受博莱霉素诱导的急性肺损伤，但不能保护小鼠免受博莱霉素或腺病毒 TGF-β1 诱导的肺纤维化。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-09-05 DOI: 10.1002/eji.202451323

Marie T. Moog, Melina Baltes, Tina Röpke, Franziska Aschenbrenner, Regina Maus, Jennifer Stolper, Danny Jonigk, Immo Prinz, Martin Kolb, Ulrich A. Maus

{"title":"Innate T-cell-derived IL-17A/F protects from bleomycin-induced acute lung injury but not bleomycin or adenoviral TGF-β1-induced lung fibrosis in mice","authors":"Marie T. Moog, Melina Baltes, Tina Röpke, Franziska Aschenbrenner, Regina Maus, Jennifer Stolper, Danny Jonigk, Immo Prinz, Martin Kolb, Ulrich A. Maus","doi":"10.1002/eji.202451323","DOIUrl":"10.1002/eji.202451323","url":null,"abstract":"The pathobiology of IL-17 in lung fibrogenesis is controversial. Here we examined the role of IL-17A/F in bleomycin (BLM) and adenoviral TGF-β1-induced lung fibrosis in mice. In both experimental models, WT and IL17af−/− mice showed increased collagen contents and remodeled lung architecture as assessed by histopathological examination, suggesting that IL-17A/F is dispensable for lung fibrogenesis. However, IL17af−/− mice responded to the BLM challenge with perturbed lung leukocyte subset recruitment. More specifically, bleomycin triggered angiocentric neutrophilic infiltrations of the lung accompanied by increased mortality of IL17af−/− but not WT mice. WT bone marrow transplantation failed to correct this phenotype in BLM-challenged IL17af−/− mice. Conversely, IL17a/f−/− bone marrow transplantation → WT did not perturb lung leukocytic responses upon BLM. At the same time, IL17af−/− mice treated with recombinant IL-17A/F showed an attenuated lung inflammatory response to BLM. Together, the data show that the degree of BLM-driven acute lung injury was critically dependent on the presence of IL-17A/F, while in both models, the fibrotic remodeling process was not.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131360","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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Antibody density on bacteria regulates C1q recruitment by monoclonal IgG but not IgM 细菌上的抗体密度能调节单克隆 IgG 的 C1q 招募，但不能调节 IgM 的招募。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-09-04 DOI: 10.1002/eji.202451228

Nathan Aymerich, Luca J. Schlotheuber, Olivia T. M. Bucheli, Kevin Portmann, Jean Baudry, Klaus Eyer

{"title":"Antibody density on bacteria regulates C1q recruitment by monoclonal IgG but not IgM","authors":"Nathan Aymerich, Luca J. Schlotheuber, Olivia T. M. Bucheli, Kevin Portmann, Jean Baudry, Klaus Eyer","doi":"10.1002/eji.202451228","DOIUrl":"10.1002/eji.202451228","url":null,"abstract":"Antibodies that trigger the complement system play a pivotal role in the immune defense against pathogenic bacteria and offer potential therapeutic avenues for combating antibiotic-resistant bacterial infections, a rising global concern. To gain a deeper understanding of the key parameters regulating complement activation by monoclonal antibodies, we developed a novel bioassay for quantifying classical complement activation at the monoclonal antibody level, and employed this assay to characterize rare complement-activating antibacterial antibodies on the single-antibody level in postimmunization murine antibody repertoires. We characterized monoclonal antibodies from various antibody isotypes against specific pathogenic bacteria (Bordetella pertussis and Neisseria meningitidis) to broaden the scope of our findings. We demonstrated activation of the classical pathway by individual IgM- and IgG-secreting cells, that is, monoclonal IgM and IgG2a/2b/3 subclasses. Additionally, we could observe different epitope density requirements for efficient C1q binding depending on antibody isotype, which is in agreement with previously proposed molecular mechanisms. In short, we found that antibody density most crucially regulated C1q recruitment by monoclonal IgG isotypes, but not IgM isotypes. This study provides additional insights into important parameters for classical complement initiation by monoclonal antibodies, a knowledge that might inform antibody screening and vaccination efforts.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 11","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.202451228","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131316","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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Colony stimulating factor 1 receptor (Csf1r) expressing cell ablation in mafia (macrophage-specific Fas-induced apoptosis) mice alters monocyte landscape and atherosclerotic lesion characteristics mafia（巨噬细胞特异性 Fas 诱导凋亡）小鼠中表达集落刺激因子 1 受体（Csf1r）的细胞消融会改变单核细胞分布和动脉粥样硬化病变特征。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-09-04 DOI: 10.1002/eji.202350943

Indira Medina, Elias B Wieland, Lieve Temmerman, Jeroen J.T. Otten, Beatriz Bermudez, Ilze Bot, Timo Rademakers, Erwin Wijnands, Leon Schurgers, Barend Mees, Theo J.C. van Berkel, Pieter Goossens, Erik A.L. Biessen

{"title":"Colony stimulating factor 1 receptor (Csf1r) expressing cell ablation in mafia (macrophage-specific Fas-induced apoptosis) mice alters monocyte landscape and atherosclerotic lesion characteristics","authors":"Indira Medina, Elias B Wieland, Lieve Temmerman, Jeroen J.T. Otten, Beatriz Bermudez, Ilze Bot, Timo Rademakers, Erwin Wijnands, Leon Schurgers, Barend Mees, Theo J.C. van Berkel, Pieter Goossens, Erik A.L. Biessen","doi":"10.1002/eji.202350943","DOIUrl":"10.1002/eji.202350943","url":null,"abstract":"Macrophage infiltration and accumulation in the atherosclerotic lesion are associated with plaque progression and instability. Depletion of macrophages from the lesion might provide valuable insights into plaque stabilization processes. Therefore, we assessed the effects of systemic and local macrophage depletion on atherogenesis. To deplete monocytes/macrophages we used atherosclerosis-susceptible Apoe−/− mice, bearing a MaFIA (macrophage-Fas-induced-apoptosis) suicide construct under control of the Csf1r (CD115) promotor, where selective apoptosis of Csf1r-expressing cells was induced in a controlled manner, by administration of a drug, AP20187. Systemic induction of apoptosis resulted in a decrease in lesion macrophages and smooth-muscle cells. Plaque size and necrotic core size remained unaffected. Two weeks after the systemic depletion of macrophages, we observed a replenishment of the myeloid compartment. Myelopoiesis was modulated resulting in an expansion of CSF1Rlo myeloid cells in the circulation and a shift from Ly6chi monocytes toward Ly6cint and Ly6clo populations in the spleen. Local apoptosis induction led to a decrease in plaque burden and macrophage content with marginal effects on the circulating myeloid cells. Local, but not systemic depletion of Csf1r+ myeloid cells resulted in decreased plaque burden. Systemic depletion led to CSF1Rlo-monocyte expansion in blood, possibly explaining the lack of effects on plaque development.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 11","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.202350943","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131359","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. 9'24 封面故事Eur.J. Immunol.9'24

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-09-04 DOI: 10.1002/eji.202470091

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Issue Information: Eur. J. Immunol. 9'24 发行信息： Eur.J. Immunol.

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-09-04 DOI: 10.1002/eji.202470092

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Impressum 印象深刻

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-09-04 DOI: 10.1002/eji.202470093

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In memory of Prof. Dr. Marcus Groettrup (1964–2022) 纪念马库斯-格罗特鲁普教授（1964-2022）博士

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-09-04 DOI: 10.1002/eji.202451341

Michael Basler, Christopher Schliehe

引用次数: 0

CD38high/HLA-DR+CD8+ T lymphocytes display pathogen-specific expansion regardless of hemophagocytic lymphohistiocytosis CD38高/HLA-DR+CD8+T淋巴细胞显示出病原体特异性扩增，与嗜血细胞性淋巴组织细胞增多症无关。

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2024-09-03 DOI: 10.1002/eji.202451140

Lorenzo Lodi, Walter Maria Sarli, Silvia Ricci, Laura Pisano, Silvia Boscia, Maria Vincenza Mastrolia, Sara Malinconi, Eleonora Fusco, Elena Sieni, Giuseppe Indolfi, Gabriele Simonini, Luisa Galli, Chiara Azzari

{"title":"CD38high/HLA-DR+CD8+ T lymphocytes display pathogen-specific expansion regardless of hemophagocytic lymphohistiocytosis","authors":"Lorenzo Lodi, Walter Maria Sarli, Silvia Ricci, Laura Pisano, Silvia Boscia, Maria Vincenza Mastrolia, Sara Malinconi, Eleonora Fusco, Elena Sieni, Giuseppe Indolfi, Gabriele Simonini, Luisa Galli, Chiara Azzari","doi":"10.1002/eji.202451140","DOIUrl":"10.1002/eji.202451140","url":null,"abstract":"The characteristic expansion of T CD38high/HLA-DR+CD8+ lymphocytes observed in hemophagocytic lymphohistiocytosis (HLH) and macrophage activation syndrome (MAS) proved able to distinguish HLH/MAS from sepsis and systemic juvenile idiopathic arthritis. However, the performance of this marker in differentiating HLH/MAS from other pediatric febrile conditions with similar clinical onset and yet entirely different treatments remains unexplored. CD38high/HLA-DR+CD8+ frequencies measured in the peripheral fresh blood of pediatric patients attended for suspicion of HLH/MAS were retrospectively recorded and clinical characteristics were retrieved. CD38high/HLA-DR+CD8+ frequencies in HLH/MAS patients (15 patients; median: 22.0%, IQR: 11.0–49.0%) were compared with those who presented febrile conditions other-than-HLH (28 patients; median: 13.0%, IQR: 3.9–28.7%; p = 0.24). HLH and non-HLH patients were subsequently regrouped based on the presence of an identified infection (22 patients; median: 27.0%, IQR: 15.2-72.1%) and compared with those without infections (21 patients; median: 7.6%, IQR: 3.7–24.3%; p = 0.0035). CD38high/HLA-DR+CD8+ percentages were significantly higher only in the infection group compared with the noninfection one, with a patent pathogen-specific expansion in Epstein–Barr virus primoinfection and visceral leishmaniasis regardless of the presence of HLH. CD38high/HLA-DR+CD8+ frequencies do not appear as an HLH-specific marker as they naturally expand in other clinical situations that are common in childhood and may mimic HLH initial presentation.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 11","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.202451140","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142124367","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