Immunology letters最新文献

{"title":"Innate Lymphoid Cells and diet: the multitask cells in metabolic syndrome progression.","authors":"Letícia Yurie Aoki, Gabriela Camargo Zicman, Luísa Menezes-Silva, Marcella Cipelli, Niels Olsen Saraiva Camara","doi":"10.1016/j.imlet.2026.107237","DOIUrl":"https://doi.org/10.1016/j.imlet.2026.107237","url":null,"abstract":"<p><p>Innate lymphoid cells (ILCs) are innate-like lymphocytes that contribute to tissue homeostasis, barrier immunity, inflammation, and host defense. In metabolic syndrome (MetS), a condition estimated to affect more than 1.5 billion adults worldwide, dietary patterns and gut microbial metabolites are increasingly recognized as regulators of immune and metabolic dysfunction [1-8]. This review critically summarizes mainly experimental and preclinical evidence, with selected human observations where available, linking dietary components, gut microbiota-derived metabolites, and ILC subsets to obesity, insulin resistance, type 2 diabetes mellitus (T2DM), and related metabolic complications. Current evidence suggests that dietary fibers, short-chain fatty acids, lipids, vitamins, and fermented foods can modulate ILC1, ILC2, and ILC3 responses in a context-dependent manner. However, most mechanistic data derive from mouse models, and direct translation to human MetS remains limited. Through integrating diet-microbiota interactions, ILC subset biology, and metabolic inflammation, this review highlights candidate pathways and biomarkers that may guide future therapeutic studies rather than established clinical interventions.</p>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":" ","pages":"107237"},"PeriodicalIF":3.2,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148818341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond the M-spike - immunoparesis and multiple myeloma. A narrative review.","authors":"Elizabeth Sarah Mayne, Catherine Mary Worsley, Tracey Monica Wiggill","doi":"10.1016/j.imlet.2026.107236","DOIUrl":"10.1016/j.imlet.2026.107236","url":null,"abstract":"<p><p>Secondary immunodeficiency or immunoparesis is an acquired impairment of the immune system which is a recognised feature of multiple myeloma (MM). Although classically described as a reduced production of polyclonal immunoglobulins, MM induces global immune dysfunction with defects in innate immune and T cell effector function. Immunoparesis can be detected in premalignant states, including monoclonal gammopathy of uncertain significance. Patients with immunoparesis have a poorer prognosis and present with severe, recurrent infection, which is associated with increased morbidity and mortality especially in the first 3 months following diagnosis, with relapse or progression and with the use of novel therapeutics. Bacterial infections, and specifically pneumonia, are the commonest presentation although there are increased risks of both viral reactivation and invasive fungal infection. Management of immunoparesis in MM includes the use of antimicrobial prophylaxis, and immunoglobulin replacement therapy particularly during high-risk periods. Although vaccination against encapsulated organisms, reactivation viruses, and circulating seasonal viruses is recommended, the response in MM may be suboptimal.</p>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":" ","pages":"107236"},"PeriodicalIF":3.2,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148818357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Killing to cure: harnessing poxvirus-driven cell death for viral immunotherapy.","authors":"April D'Arcy, Brian J Ferguson","doi":"10.1016/j.imlet.2026.107235","DOIUrl":"https://doi.org/10.1016/j.imlet.2026.107235","url":null,"abstract":"<p><p>Oncolytic virotherapy represents a promising frontier in cancer immunotherapy, leveraging the ability of oncolytic viruses (OVs) to selectively replicate within tumour cells and induce antitumour immunity. In this review, we focus on the clinical development of oncolytic poxviruses and propose that understanding fundamental mechanisms of poxvirus-induced cell death can inform rational clinical development strategies that may avoid challenges and improve outcomes in viral immunotherapy. We discuss the development of Olvimulogene nanivacirepvec (Olvi-Vec), Pexastimogene devacirepvec (Pexa-Vec), and other candidates; the basic biology of poxviruses; their manipulation of host antiviral defences; and the pathways of regulated cell death they can induce, including apoptosis, necroptosis, pyroptosis, and ferroptosis. We examine the potential for optimising oncolysis through targeted genetic modification and combination therapy, with the aim of enhancing the immunogenicity of cell death to overcome the immunosuppressive tumour microenvironment and to enhance adaptive antitumour immune responses.</p>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":" ","pages":"107235"},"PeriodicalIF":3.2,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148812865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Innate lymphoid cells: Bridging basic biology and disease.","authors":"Metin Yusuf Gelmez, Fatma Betul Oktelik, Aysenur Kokoglu, Semra Demir, Suzan Cinar, Gunnur Deniz","doi":"10.1016/j.imlet.2026.107226","DOIUrl":"10.1016/j.imlet.2026.107226","url":null,"abstract":"<p><p>Innate lymphoid cells (ILCs) lack antigen-specific receptors and are, consequently, distinct from conventional T and B lymphocytes. Nevertheless, they play a critical role in immune regulation through the rapid secretion of effector cytokines. Due to these functional properties, ILCs exhibit remarkable similarities to CD4⁺ T helper lymphocytes. With the inclusion of natural killer (NK) cells in the current ILC classification, ILCs are now considered the innate immune system counterparts of adaptive T lymphocytes. Recent studies have demonstrated that ILCs are essential for maintaining tissue homeostasis, particularly at mucosal surfaces, and their dysregulation is closely linked to the pathogenesis of inflammatory, autoimmune and allergic diseases. Beyond their roles in chronic inflammation, ILCs act as pivotal integrators of dietary, microbial, and neuroendocrine signals within specialized tissue microenvironments. In allergic diseases and asthma, ILC2s initiate early type 2 responses, while in the intestinal mucosa, plasticity between ILC3 and ILC1 subsets critically regulates the balance between homeostasis and inflammatory bowel disease (IBD). Additionally, ILCs are emerging as significant players in tumor immunology, exhibiting both pro- and anti-tumorigenic roles depending on the tumor microenvironment. This review provides a comprehensive overview of ILC biology, their tissue-specific functions, and their involvement in immune-mediated disorders. Moreover, we discuss the therapeutic potential of targeting ILCs, including cell-based approaches and their significance as biomarkers, to establish a framework for next-generation precision immunotherapies.</p>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":" ","pages":"107226"},"PeriodicalIF":3.2,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148706342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PD-L1 expression in cervical cancer tissue is strongly associated with the expression of CD73/TGF-β1, the percentage of CD8+/PD-1+ T cells and disease progression","authors":"Muñóz-Godínez Ricardo ,&nbsp;Monroy-García Alberto ,&nbsp;Hernández-Cueto Ángeles María ,&nbsp;García-Rocha Rosario ,&nbsp;Weiss-Steider Benny ,&nbsp;Hernández-Montes Jorge ,&nbsp;Don-López Christian Azucena ,&nbsp;Díaz Ramos Juan Antonio ,&nbsp;Pérez-Koldenkova Vadim ,&nbsp;Molina-Castillo Gabriela ,&nbsp;Mora-García María de Lourdes","doi":"10.1016/j.imlet.2026.107150","DOIUrl":"10.1016/j.imlet.2026.107150","url":null,"abstract":"<div><div>The PD-1/PD-L1 signaling pathway plays a pivotal role in dampening anti-tumor immune responses. We previously reported that adenosine (Ado) increases the expression of programmed death ligand 1 (PD-L1) in cervical cancer (CC) cells by inducing TGF-β production. We also showed that supernatants from Ado-treated CC cells increased programmed cell death protein 1 (PD-1) expression in CD8+ <em>T</em> lymphocytes. In this study, we investigated the associations between PD-L1, CD73, and TGF-β expression and the percentage of PD-1-expressing CD8+ <em>T</em> lymphocytes in cervical tissue samples from normal donors (NDs), as well as patients with cervical intraepithelial neoplasia (CIN-I, CIN-II, CIN-III) and cervical cancer (CC). This retrospective observational study analyzed biopsies from untreated patients with CIN-1 (<em>n</em> = 27), CIN-II (<em>n</em> = 25), CIN-III (<em>n</em> = 23), and CC (<em>n</em> = 23), in addition to ND tissue samples (<em>n</em> = 30) as controls. Tissue microarrays (TMAs) were generated in triplicate and stained with anti-PD-L1, anti-CD73, anti-TGF-β1, anti-PD-1, and anti-CD8 monoclonal antibodies. Our results showed that the expression of PD-L1, CD73, and TGF-β1, along with the percentage of CD8+/PD-1 + <em>T</em> cells, increased in cervical tissues, correlating with disease progression. PD-L1 expression positively correlated with both CD73 (<em>r</em> = 0.8274, <em>p</em> &lt; 0.001) and TGF-β1 (<em>r</em> = 0.8535, <em>p</em> &lt; 0.001). Interestingly, the coexpression of PD-L1 and TGF-β1 in cervical tissues from patients with CIN-III and CC markedly increased. Furthermore, the percentage of CD8+ cells positively correlated with PD-1 expression (<em>r</em> = 0.7199, <em>p</em> &lt; 0.01). These findings suggest that the expression of PD-L1 and PD-1 in CC tissues is strongly correlated with the expression of CD73 and TGF-β1. Therefore, the joint analysis of these biomarkers could be highly useful for evaluating disease prognosis and for developing strategies to improve the efficacy of immunotherapy protocols in CC patients treated with immune checkpoint inhibitors (ICIs).</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"280 ","pages":"Article 107150"},"PeriodicalIF":2.8,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146219162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of computed tomography densitometry with disease progression and spatial heterogeneity in rheumatoid arthritis-associated interstitial lung disease","authors":"Zhinan Guo ,&nbsp;Yu Zhang ,&nbsp;Guanheng Li ,&nbsp;Nie Han ,&nbsp;Xingting Jiang ,&nbsp;Jiawei Ma ,&nbsp;Yayi Qin ,&nbsp;Diru Zhu ,&nbsp;Xiaoli Gu ,&nbsp;Lin Jin","doi":"10.1016/j.imlet.2026.107157","DOIUrl":"10.1016/j.imlet.2026.107157","url":null,"abstract":"<div><h3>Objectives</h3><div>This study aimed to assess the efficacy of quantitative computed tomography (qCT) in distinguishing rheumatoid arthritis-associated interstitial lung disease (RA-ILD) and monitoring its progression.</div></div><div><h3>Methods</h3><div>HRCT images of 138 RA-ILD patients (GAP_I, <em>n</em> = 90; GAP_II+III, <em>n</em> = 48) and 47 RA controls were retrospectively analyzed. The normal lung attenuation areas (NL%), the percentage of low attenuation areas (LAA%), and the percentage of high-attenuation areas (HAA%) were measured for each lung lobe. Correlations between qCT indices and pulmonary function tests were evaluated using Spearman’s rank correlation. ROC curves tested the discriminative performance of qCT indices. Multivariable logistic regression assessed associations between qCT indices and RA-ILD.</div></div><div><h3>Results</h3><div>The NL% decreased, while the LAA% and HAA% increased in the early and moderate-to-advanced stages of ILD, respectively (<em>p</em> &lt; 0.05). Multivariate regression identified HAA% as an independent risk factor for ILD staging (OR: 1.737, 95% CI: 1.182–2.551, <em>p</em> = 0.005). When combining NL%, LAA%, and HAA%, the AUCs for early diagnosis and progression monitoring were 0.760 and 0.773, respectively (<em>p</em> &lt; 0.05). RA-ILD exhibited spatial heterogeneity, with the lower lobes being primarily affected.</div></div><div><h3>Conclusions</h3><div>Quantitative parameters can effectively differentiate early-stage RA-ILD and monitor its progression. LAA% is significantly correlated with early diagnosis, whereas HAA% demonstrates higher specificity in later stages. Quantitative lung densitometry may prove to be a valuable tool for clinical decision-making.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"280 ","pages":"Article 107157"},"PeriodicalIF":2.8,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147344087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin D ameliorates NETosis and Th17/Treg imbalance in experimental autoimmune thyroiditis","authors":"Hai-Yan Yang ,&nbsp;Xi-Zhen Wu ,&nbsp;Yu-Ping Liu ,&nbsp;Gui-Yang Jiang ,&nbsp;Ying-Fen Qin ,&nbsp;Xing-Huan Liang ,&nbsp;Zuo-Jie Luo","doi":"10.1016/j.imlet.2026.107156","DOIUrl":"10.1016/j.imlet.2026.107156","url":null,"abstract":"<div><h3>Background</h3><div>Neutrophil extracellular traps (NETs) have been implicated in various autoimmune diseases; however, their role in Hashimoto's thyroiditis (HT) remains poorly understood. This study aimed to characterize NETs formation, explore its association with thyroid dysfunction and adaptive immunity, and evaluate the therapeutic potential of vitamin D (VD) in experimental autoimmune thyroiditis (EAT).</div></div><div><h3>Methods</h3><div>EAT was induced in BALB/c mice via thyroglobulin immunization combined with excess iodine intake. The VD group received additional intraperitoneal calcitriol supplementation. Thyroid histopathology, MHC-II expression, thyroid antibodies (TGAb and TPOAb), plasma DNase-I and 1,25(OH)₂D₃ levels, NETs formation, and splenic T cell subsets (Th17, Treg, Th1, Th2) and cytokines were assessed. Parallel experiments were conducted using neutrophils isolated from HT patients.</div></div><div><h3>Results</h3><div>Neutrophils from both EAT mice and HT patients exhibited enhanced NETosis compared to controls. EAT mice showed lower levels of DNase-I, 1,25(OH)₂D₃, Treg, and Th1 cells, along with higher Th17 and Th2 cells, elevated Th17/Treg ratio, and heightened thyroid MHC-II expression. NETs levels positively correlated with Th17, Th2, and MHC-II expression, and negatively with Treg, Th1, 1,25(OH)₂D₃, and DNase-I. VD supplementation mitigated thyroiditis and TPOAb levels, suppressed NETs formation, and reduced the Th17/Treg ratio and IL-17 levels.</div></div><div><h3>Conclusions</h3><div>NETs contribute to Th17 bias and MHC-II over-expression in HT, suggesting a role in shaping the adaptive immune response. Vitamin D restrains NETosis and restores T-cell homeostasis, highlighting its potential as an adjunctive therapy for HT.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"280 ","pages":"Article 107156"},"PeriodicalIF":2.8,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147344083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Src-family kinase control of CAR signaling: the paradoxical and multifaceted role of LCK","authors":"Luca Simeoni ,&nbsp;Dimitrios Mougiakakos ,&nbsp;Stephan Fricke","doi":"10.1016/j.imlet.2026.107158","DOIUrl":"10.1016/j.imlet.2026.107158","url":null,"abstract":"<div><div>Lymphocyte-specific protein tyrosine kinase (LCK) is central to early T-cell receptor (TCR) signaling and is tightly regulated by phosphorylation, protein–protein interactions, and spatial organization to control T-cell activation and fate. Chimeric antigen receptors (CARs) co-opt core elements of the TCR signaling machinery, including LCK. Nevertheless, important mechanistic differences, which remain largely unexplored, exist in how LCK is recruited, activated, and restrained during CAR signaling relative to canonical TCR signaling. Accumulating evidence indicates that CAR architecture, particularly the nature and organization of costimulatory signaling domains, profoundly influences LCK activity, signal strength, tonic signaling, and downstream differentiation outcomes. Excessive or sustained LCK activity can drive metabolic stress and exhaustion, whereas limiting or fine-tuning LCK signaling improves CAR T-cell persistence and therapeutic efficacy. Here, we review the current understanding of LCK regulation in CAR signaling and highlight recent insights into pharmacologic and structural strategies to tune LCK activity. A deeper understanding of LCK regulation is essential for improving the efficacy and safety of CAR T cells and may help in the design of next-generation CARs.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"280 ","pages":"Article 107158"},"PeriodicalIF":2.8,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147365147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Control of regulatory T cell differentiation and function by glycan remodeling","authors":"Yanwen Wang ,&nbsp;Yunyue Shen ,&nbsp;Kaini Liu ,&nbsp;Rui Liang ,&nbsp;Fangkang Meng ,&nbsp;Rongliang Zhang ,&nbsp;Ziqi Jiang ,&nbsp;Aiting Wang ,&nbsp;Jieqiong Chen ,&nbsp;Yangyang Li","doi":"10.1016/j.imlet.2026.107138","DOIUrl":"10.1016/j.imlet.2026.107138","url":null,"abstract":"<div><div>Regulatory T (Treg) cells are indispensable for peripheral tolerance and immune homeostasis. Protein glycosylation plays an essential role in various cellular functions of T cells, including T cell development, thymocyte selection, T cell activation and differentiation. Recently, many studies have explored the effects of glycosylation on Treg biology. Both <em>N-</em>linked glycosylation and <em>O-</em>linked glycosylation are important for the development, migration, suppressive function and lineage stability of Treg cells. In this review, we will discuss emerging evidence of glycosylation regulations on Treg cells and the developing technologies on the detection and analysis of unique glycan patterns and branching features. These efforts will help to reveal the function and regulatory roles of glycan remodeling in Treg cells, explore how glycan patterns modulate their phenotypes, and provide a strategic basis for clinical intervention and therapy of inflammatory diseases by targeting key glycosylation molecules in Treg cells.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"279 ","pages":"Article 107138"},"PeriodicalIF":2.8,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145966066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Escherichia coli J5-derived OMVs with hypoendotoxic LPS: Potential boosters of T-cell immunity and IL-17 production for enhanced vaccine efficacy","authors":"Jiawen Zhang ,&nbsp;Yuhang Zhi ,&nbsp;Wenzhu Yin ,&nbsp;Haiyan Wang ,&nbsp;Yu Lu ,&nbsp;Fang Ma ,&nbsp;Deyun Wang","doi":"10.1016/j.imlet.2026.107137","DOIUrl":"10.1016/j.imlet.2026.107137","url":null,"abstract":"<div><div>Lipopolysaccharide (LPS) is the core epitope of <em>Escherichia coli</em> (<em>E. coli</em>) J5 (O111:B4), a vaccine strain for bovine mastitis. It provides a significant protective effect in host suffering from Gram-negative bacteremia. However, LPS remains the main toxin in bacterial outer membrane vesicles (OMVs), which are non-replicative nanoparticles capable of robust immune modulation. Here, we focused on the immunomodulatory effect of hypoendotoxic LPS containing penta-acylated monophosphoryl lipid A on OMVs derived from <em>E. coli</em> J5. OMVs containing penta-acylated monophosphoryl LPS (referred to as mOMVs) induced a moderate inflammatory response. mOMVs still remained nanoparticle diameters of approximately 30 nm and 100 nm, facilitating antigen drainage to lymph nodes and presentation to dendritic cells (DCs). OMVs could stimulate cell aggregation at injection sites, conducive to DCs activation, with mOMVs enhancing CD3⁺ <em>T</em> cell proliferation and differentiation of CD4⁺ and CD8⁺ <em>T</em> cell. Notably, CD4⁺ <em>T</em> cells activated by DCs primed with mOMVs produced higher levels of IL-17, suggesting potential enhanced mucosal immunity. Additionally, mOMVs elicited protective antibody responses against clinically isolated <em>E. coli</em> strain. These findings suggest that detoxified LPS endows OMVs with increased efficacy and safety, thereby further promoting the optimization of these vesicles for inducing cross-protection.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"279 ","pages":"Article 107137"},"PeriodicalIF":2.8,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145917523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}