{"title":"In vitro modulation of T cells in myasthenia gravis by low-dose IL-2","authors":"Merve Çebi, Arman Çakar, Hacer Durmuş, Onur Akan, Fikret Aysal, Yeşim Parman, Güher Saruhan-Direskeneli","doi":"10.1002/eji.202451268","DOIUrl":"10.1002/eji.202451268","url":null,"abstract":"<p>Follicular helper (Tfh), peripheral helper (Tph), and regulatory (Treg) T cells are involved in myasthenia gravis (MG) pathogenesis, an autoimmune disorder arising from autoantibodies targeting neuromuscular junction proteins. This study explores the impact of low-dose IL-2 on Tfh, Tph, and Treg cells in vitro in MG. Acetylcholine-receptor antibody-positive MG (AChR-MG), muscle-specific kinase antibody-positive MG (MuSK-MG) patients, and healthy controls (HC) were studied. Blood cells were cultured with/without IL-2 and compared by the ratios of IL-2 stimulated/unstimulated cultures. In both AChR-MG and MuSK-MG patients, CD25<sup>+</sup>FoxP3<sup>+</sup>Tregs were lower, while CXCR5<sup>+</sup>PD-1<sup>+</sup> or ICOS<sup>+</sup>Tfh and CXCR5<sup>−</sup>PD-1<sup>+</sup> or ICOS<sup>+</sup>Tph cells were higher compared with HC. Among the MG group, the FoxP3<sup>+</sup> Treg cells in AChR-MG patients were even lower compared with MuSK-MG patients. In vitro IL-2 stimulation increased Tregs in all groups while decreasing PD-1<sup>+</sup>/ICOS<sup>+</sup>Tfh and PD-1<sup>+</sup>/ICOS<sup>+</sup>Tph populations. The fold-increase ratio of Tregs and the fold-decrease ratio of PD-1<sup>+</sup> or ICOS<sup>+</sup>Tfh and ICOS<sup>+</sup>Tph cells in AChR-MG and MuSK-MG patients were greater than in HCs. Low-dose IL-2 treatment may balance Tfh, Tph, and Treg cells in MG patients, offering a potential opportunity for disease modulation.</p>","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"54 11","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.202451268","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142268289","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}
{"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":"<p>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.</p>","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}
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":"<p>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 (<i>Bordetella pertussis</i> and <i>Neisseria meningitidis</i>) 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.</p>","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}
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":"<p>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 <i>Apoe<sup>−</sup></i><sup>/−</sup> mice, bearing a MaFIA (macrophage-Fas-induced-apoptosis) suicide construct under control of the <i>Csf1r</i> (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 CSF1R<sup>lo</sup> myeloid cells in the circulation and a shift from Ly6c<sup>hi</sup> monocytes toward Ly6c<sup>int</sup> and Ly6c<sup>lo</sup> 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 <i>Csf1r</i><sup>+</sup> myeloid cells resulted in decreased plaque burden. Systemic depletion led to CSF1R<sup>lo</sup>-monocyte expansion in blood, possibly explaining the lack of effects on plaque development.</p>","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}
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":"<p>The characteristic expansion of T CD38<sup>high</sup>/HLA-DR<sup>+</sup>CD8<sup>+</sup> 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. CD38<sup>high</sup>/HLA-DR<sup>+</sup>CD8<sup>+</sup> frequencies measured in the peripheral fresh blood of pediatric patients attended for suspicion of HLH/MAS were retrospectively recorded and clinical characteristics were retrieved. CD38<sup>high</sup>/HLA-DR<sup>+</sup>CD8<sup>+</sup> 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%; <i>p</i> = 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%; <i>p</i> = 0.0035). CD38<sup>high</sup>/HLA-DR<sup>+</sup>CD8<sup>+</sup> 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. CD38<sup>high</sup>/HLA-DR<sup>+</sup>CD8<sup>+</sup> 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.</p>","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}
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":"<p>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 <i>IL6, ADIPOQ</i>, <i>FABP4, LPL, PPARG</i>, and <i>CD36</i> in normal tissue were associated with worse overall survival of patients with ER-positive breast cancer. In tissue with higher expression of <i>IL6</i> and <i>ADIPOQ</i>, 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.</p>","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}
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":"<p>Lymphotoxin α and lymphotoxin β (LTs), TNF superfamily members, are expressed in either soluble (LTα<sub>3</sub>) or membrane-bound (LTα<sub>1</sub>β<sub>2</sub> or LTα<sub>2</sub>β<sub>1</sub>) 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 T<sub>H</sub> cells in the CNS. In contrast, T-cell-derived lymphotoxins promoted IL-17A- and GM-CSF-mediated T<sub>H</sub> 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.</p>","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}
{"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":"<p>Dectin-1 is a C-type lectin-receptor involved in sensing fungi by innate immune cells. Encoded by the <i>Clec7a</i> 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 <i>Clec7a</i> gene, leading to a non-sense Dectin-1a mRNA in C57BL/6 mice. Using backcrossing, we generated mice with the C57BL/6 <i>Clec7a</i> 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.</p>","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}
{"title":"Expansion of human γδ T cells in periphery: Lessons learned from development, infections, and compromised thymic function","authors":"Sarina Ravens, Eva Tolosa","doi":"10.1002/eji.202451073","DOIUrl":"10.1002/eji.202451073","url":null,"abstract":"<p>γδ T cells predominantly develop in the fetal period. Post birth they respond swiftly to environmental insults, pathogens and tumors, especially when other immune effector cells are less ready to function. Most of our understanding of γδ T-cell development, peripheral adaptation, and function derives from murine studies. The recent advancement of immunological methods allows now to decipher human γδ T-cell biology in patient cohorts and tissue samples, and to manipulate them using in vitro systems. In this review, we summarize γδ T-cell development in the human thymus, their functional adaptation to the microbial environment from birth until old age, and their capacity to expand and fill up the peripheral niche under conditions of perturbations of conventional T-cell development.</p>","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.202451073","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142078541","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}
Paolo Ripellino, Bettina Schreiner, Daniela Latorre
{"title":"Expanding our understanding of Guillain–Barré syndrome: Recent advances and clinical implications","authors":"Paolo Ripellino, Bettina Schreiner, Daniela Latorre","doi":"10.1002/eji.202250336","DOIUrl":"10.1002/eji.202250336","url":null,"abstract":"<p>Guillain–Barré syndrome (GBS) is a rare yet potentially life-threatening disorder of the peripheral nervous system (PNS), characterized by substantial clinical heterogeneity. Although classified as an autoimmune disease, the immune mechanisms underpinning distinct GBS subtypes remain largely elusive. Traditionally considered primarily antibody-mediated, the pathophysiology of GBS lacks clarity, posing challenges in the development of targeted and effective treatments. Nevertheless, recent investigations have substantially expanded our understanding of the disease, revealing an involvement of autoreactive T cell immunity in a major subtype of GBS patients and opening new biomedical perspectives. This review highlights these discoveries and offers a comprehensive overview of current knowledge about GBS, including ongoing challenges in disease management.</p>","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.202250336","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142071558","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}