Immunology letters最新文献

{"title":"Design and application of a multi-epitope ACE2 antigen for detection of autoantibodies in post-COVID-19 diagnosed type 1 diabetes","authors":"Maryam Marzban ,&nbsp;Nayebali Ahmadi ,&nbsp;Fattah Sotoodehnejadnematalahi ,&nbsp;Alireza Gholami","doi":"10.1016/j.imlet.2025.107127","DOIUrl":"10.1016/j.imlet.2025.107127","url":null,"abstract":"<div><h3>Background</h3><div>Type 1 diabetes mellitus (T1DM) is an autoimmune condition involving pancreatic β-cell destruction. Recent publications associate SARS-CoV-2 infection with autoimmune activation and the development of de novo Type 1 Diabetes Mellitus (T1DM), possibly via molecular mimicry, inflammation, and direct β-cell damage. The angiotensin-converting enzyme 2 (ACE2) receptor, exploited by SARS-CoV-2 for cellular entry, is present in pancreatic islets and may be susceptible to autoantibody attack. This study was done to assess anti-ACE2 autoantibody titers in newly diagnosed patients with T1DM post-COVID-19 infection.</div></div><div><h3>Methods</h3><div>Blood samples were collected from thirty-five patients with new-onset T1DM post-COVID-19 and thirty healthy controls who recovered from COVID-19. Bioinformatic epitope prediction software was used to construct an eleven-epitope multi-epitope antigen of ACE2. The recombinant was cloned into BL21 E. coli via pET-32a+ vector, expressed, purified by affinity chromatography, and verified by Western blotting. Indirect ELISA was established to measure anti-ACE2 antibodies, and the Mann-Whitney test was applied for statistical comparison.</div></div><div><h3>Results</h3><div>The designed multi-epitope vaccine had significant structural stability and effective expression. ELISA results demonstrated significantly higher anti-ACE2 autoantibody levels in T1DM patients compared with the control group (p = 0.01).</div></div><div><h3>Conclusion</h3><div>The results are consistent with a potential association between SARS-CoV-2 infection and the onset of T1DM by autoimmune responses against ACE2. Very high levels of anti-ACE2 antibodies may cause β-cell dysfunction and insulin deficiency. More longitudinal studies are required to establish causality and investigate anti-ACE2 as a prospective biomarker for post-COVID autoimmune diabetes.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"279 ","pages":"Article 107127"},"PeriodicalIF":2.8,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145888878","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":"Machine learning reveals sex-biased platelet-associated molecular signatures in systemic lupus erythematosus","authors":"Shuping Li ,&nbsp;Hui Ouyang ,&nbsp;Tianjiao Cui ,&nbsp;Jiawen Lin ,&nbsp;Keping Wu ,&nbsp;Enyi Zhu ,&nbsp;Yuan Sui ,&nbsp;Mingcheng Huang","doi":"10.1016/j.imlet.2026.107136","DOIUrl":"10.1016/j.imlet.2026.107136","url":null,"abstract":"<div><h3>Objectives</h3><div>Autoimmune diseases (ADs) demonstrate a higher prevalence in women than men. Systemic Lupus Erythematosus (SLE) stands out among multiple ADs as an extreme case of the imbalanced sex ratio observed at disease onset, predominantly affecting females. This discrepancy can be ascribed to genetics, hormonal influences, environmental triggers, and more. Despite numerous studies aiming to uncover the sex differences in SLE, comprehensive bioinformatics integration for understanding its biological heterogeneity remains largely unexplored.</div></div><div><h3>Methods</h3><div>Transcriptomic data of 338 individuals (175 normal and 163 SLE) from the six SLE studies (GSE154851, GSE20864, GSE99967, GSE39088, GSE72754, and GSE81622) from the Gene Expression Omnibus were analyzed to uncover sex-specific candidate genes using differential gene expression analysis. Machine learning algorithms selected the candidate genes, and their performance was evaluated using receiver operating characteristic curves. Analyses were done by ADEx, GEO2R, and scRNA-seq.</div></div><div><h3>Results</h3><div>72 enriched terms are shared between the female subgroup and the overall dataset, but none are shared between the male subgroup and the overall dataset. We identified differential expression of platelet glycoprotein VI (GP6) in male SLE, but not in the females, with GP6 predominantly expressed in platelets. Moreover, the correlation between GP6 and pre-T cell antigen receptor alpha (PTCRA) was significantly more pronounced in male SLE patients (<em>r</em> = 0.7004, <em>p</em> = 0.0053) compared to females (<em>r</em> = 0.5741, <em>p</em> &lt; 0.0001). Additionally, GP6 and PTCRA were positively associated with Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) in male SLE patients, but not in females.</div></div><div><h3>Conclusions</h3><div>There is a sex-based bias in SLE. GP6 marks a PTCRA-expressing platelet subset that is differentially altered in male SLE compared with controls, but not in female SLE, indicating a sex-dependent platelet molecular phenotype. The differential GP6 expression on PTCRA-expressing platelets between male and female SLE patients may contribute to differences in their clinical manifestations.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"279 ","pages":"Article 107136"},"PeriodicalIF":2.8,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145932778","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":"PLIN2 exacerbates Allergic Rhinitis by inhibiting PINK1/Parkin-mediated mitophagy","authors":"Wangbo Yu ,&nbsp;Shuai Zhang ,&nbsp;Lijuan Peng ,&nbsp;Jingwei Du","doi":"10.1016/j.imlet.2025.107107","DOIUrl":"10.1016/j.imlet.2025.107107","url":null,"abstract":"<div><h3>Objective</h3><div>To investigate the pro-inflammatory role and underlying mechanism of Perilipin 2 (PLIN2) in Allergic Rhinitis (AR), focusing on its regulation of PINK1/Parkin-mediated mitophagy and the subsequent impact on lipid metabolism and oxidative stress.</div></div><div><h3>Methods</h3><div>Single-cell RNA sequencing (scRNA-seq) analysis was performed using GSE261706 from the GEO database, involving nasal mucosa from AR patients and healthy controls. A murine AR model was induced by ovalbumin (OVA), and human nasal epithelial cells (HNEpCs) were stimulated with Der p1. Interventions included AAV-mediated PLIN2 knockdown in vivo and siRNA-mediated knockdown in vitro. Techniques included Western blotting, qRT-PCR, flow cytometry, ELISA, and immunofluorescence/histological staining to assess PLIN2 expression, mitophagy, lipid accumulation, oxidative stress, and inflammatory responses.</div></div><div><h3>Results</h3><div>scRNA-seq analysis identified PLIN2 as a significantly upregulated gene in AR epithelial cells, which correlated with dysfunctional autophagy pathways. In both OVA-induced mice and Der p1-treated HNEpCs, PLIN2 expression was significantly elevated, accompanied by inhibited mitophagy (decreased LC3-II/I ratio, reduced PINK1/Parkin levels, and p62 accumulation), increased lipid deposition, and elevated ROS levels. PLIN2 knockdown markedly ameliorated AR pathology in mice, reducing inflammatory infiltration and serum levels of IgE, IL-4, and IL-5. Mechanistically, PLIN2 knockdown restored PINK1/Parkin-mediated mitophagy, decreased lipid accumulation, and attenuated ROS-induced cellular damage in HNEpCs.</div></div><div><h3>Conclusions</h3><div>PLIN2 exacerbates AR pathogenesis by inhibiting PINK1/Parkin-mediated mitophagy, promoting lipid accumulation and oxidative stress, and ultimately causing cellular damage in nasal epithelial cells. PLIN2 acts as a pivotal mediator linking metabolic dysregulation to inflammation, highlighting it as a promising therapeutic target for AR treatment.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"278 ","pages":"Article 107107"},"PeriodicalIF":2.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145451700","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":"Interaction between IL-23/Th17 immune inflammatory axis and intestinal flora in gastric mucosal atrophy caused by Helicobacter pylori infection in the elderly","authors":"Haiping Shen,&nbsp;Shuyuan Zhu,&nbsp;Lingling Ren,&nbsp;Fangling Chen,&nbsp;Chengyong Qian,&nbsp;Xiangcheng Hu,&nbsp;Guanglan Chen","doi":"10.1016/j.imlet.2025.107114","DOIUrl":"10.1016/j.imlet.2025.107114","url":null,"abstract":"<div><h3>Objective</h3><div>To explore the interactive effects of the interleukin-23 (IL-23)/Th17 immune-inflammatory axis and gut microbiota in gastric mucosal atrophy among elderly patients with Helicobacter pylori (HP) infection.</div></div><div><h3>Methods</h3><div>A total of 210 elderly patients with HP infection from Lishui Second People's Hospital between January 2023 and June 2024 were selected as the study group, and 210 healthy volunteers during the same period served as the control group. The IL-23/Th17 immune-inflammatory axis factors [IL-23, interleukin-17 (IL-17), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-2 (IL-2)], and gut microbiota were compared between the study and control groups. The study group was further divided into an atrophy subgroup (101 cases) and a non-atrophy subgroup (109 cases) based on the presence of gastric mucosal atrophy. Clinical data, IL-23/Th17 immune-inflammatory axis factors, and gut microbiota characteristics were compared between the two subgroups. Logistic regression analysis was used to investigate the influencing factors of gastric mucosal atrophy in elderly patients with HP infection and the interactive effects of the IL-23/Th17 immune-inflammatory axis and gut microbiota. Receiver operating characteristic (ROC) curve and area under the curve (AUC) analyses were performed to assess the predictive value of the IL-23/Th17 immune-inflammatory axis and gut microbiota for gastric mucosal atrophy in elderly patients with HP infection.</div></div><div><h3>Results</h3><div>The study group had higher serum levels of IL-23, IL-17, TNF-α, IL-6, IL-2, and a higher count of <em>Lactobacillus acidophilus</em>, but lower counts of Bifidobacterium and Lactobacillus compared to the control group (<em>P</em> &lt; 0.05). Within the study group, the atrophy subgroup showed more pronounced differences in these immunological and microbiological parameters compared to the non-atrophy subgroup (all P &lt; 0.05). Logistic regression identified all measured immune factors and gut microbiota as independent influencing factors for gastric mucosal atrophy (all P &lt; 0.05). Significant interactive effects were observed between the IL-23/Th17 axis factors and gut microbiota (all P &lt; 0.05). The combined ROC model incorporating these factors achieved an AUC of 0.908 for predicting gastric mucosal atrophy, significantly outperforming individual predictors (all P &lt; 0.001).</div></div><div><h3>Conclusion</h3><div>There are significant interactive effects between the IL-23/Th17 immune-inflammatory axis and gut microbiota in gastric mucosal atrophy among elderly patients with HP infection, and the combined predictive value is reliable.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"278 ","pages":"Article 107114"},"PeriodicalIF":2.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145633081","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":"Dendritic Cells: key controllers of lymphoid tissue organization","authors":"Alessia Calabrò ,&nbsp;Claudia De Pasquale ,&nbsp;Fabiana Drommi ,&nbsp;Elena Giusto ,&nbsp;Silvia Tamburini ,&nbsp;Grazia Vento ,&nbsp;Sayuri Yamazaki ,&nbsp;Stefania Campana ,&nbsp;Guido Ferlazzo","doi":"10.1016/j.imlet.2025.107111","DOIUrl":"10.1016/j.imlet.2025.107111","url":null,"abstract":"<div><div>Dendritic cells (DCs) are highly efficient antigen-presenting cells that play a central role in inducing and controlling immune responses. Beyond their role in antigen presentation and in orchestrating lymphocyte activities, DCs also contribute to the spatial and functional organization of lymphoid structures, including both secondary and tertiary lymphoid organs, acting at different levels during both lymphoid tissue neogenesis and their maintenance.</div><div>DCs can facilitate lymphoid tissue development by interacting with both lymphoid tissue inducer and organizer cells, initiating early aggregation and supporting lymphotoxin-mediated signaling pathways essential for lymphoid structure maturation. Additionally, DCs release chemokines attracting and anchoring immune cells in lymphoid tissues and regulate the formation and the overall size of high endothelial venule system, which mediate immune cell trafficking into lymphoid tissues.</div><div>The dynamic crosstalk between DCs and fibroblastic reticular cells (FRC), which facilitate immune cell interactions and compartmentalization, is essential for lymphoid tissue specialization and function, though the precise cellular and molecular mechanisms of DC/FRC crosstalk remain to be fully elucidated.</div><div>Finally, studies in mice and humans suggest that DC subsets are pivotal in T follicular helper cell differentiation, essential for humoral immunity in B cell follicles of lymphoid tissues, therefore emphasizing DCs’ critical role also in supporting B cell maturation and antibody responses in the germinal centers of lymphoid organs.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"278 ","pages":"Article 107111"},"PeriodicalIF":2.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145530634","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":"Potential link between COVID-19 infection/vaccination and the onsets of TAFRO syndrome and idiopathic multicentric castleman disease","authors":"Masataka Umeda ,&nbsp;Lamiaa Mohamed ,&nbsp;Ayaka Umetsu ,&nbsp;Mizuna Otsuka ,&nbsp;Yushiro Endo ,&nbsp;Toshimasa Shimizu ,&nbsp;Shoichi Fukui ,&nbsp;Remi Sumiyoshi ,&nbsp;Tomohiro Koga ,&nbsp;Atsushi Kawakami","doi":"10.1016/j.imlet.2025.107123","DOIUrl":"10.1016/j.imlet.2025.107123","url":null,"abstract":"<div><div>COVID-19 infection and vaccination have been reported as potential triggers for various autoimmune diseases, including TAFRO syndrome and idiopathic multicentric Castleman disease (iMCD). We investigated the incidence of TAFRO syndrome and that of iMCD in the patients admitted to Nagasaki University Hospital over a 10-year period from November 2014 to October 2024. The primary endpoint was the incidences of TAFRO syndrome/iMCD before and after the COVID-19 pandemic. The secondary endpoint was the impact of COVID-19 vaccination ≤4 weeks of disease onset on the patients' prognoses. Our analyses revealed that in the 5 years and 5 month-period before the pandemic, there were seven cases of TAFRO syndrome/iMCD (1.3 cases/year), while in the 4 years and 7 month-period following the pandemic's onset, 18 cases were identified (3.9 cases/year). Specifically, for iMCD-TAFRO and TAFRO without iMCD, the incidence rose from two cases (0.4 cases/year) pre-pandemic to 11 cases (2.4 cases/year) post-pandemic, representing a marked increase. Among the 13 cases of iMCD-TAFRO and TAFRO without iMCD observed, four patients developed symptoms within 4 weeks of receiving the COVID-19 vaccine, and all required ICU admission. Conversely, among the nine patients without a recent vaccination history, only two required ICU care (<em>p</em> = 0.02). Although potential confounders which could influence the diagnosis (e.g., increased awareness of the disease) were not controlled for, our findings suggest a possible link between COVID-19 infection or vaccination and the onsets of TAFRO syndrome and iMCD. COVID-19 vaccination is a crucial public health strategy to reduce COVID-19-related death and disability, but TAFRO syndrome that develops post-vaccination may progress to severe illness requiring ICU care, highlighting the need for careful monitoring.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"278 ","pages":"Article 107123"},"PeriodicalIF":2.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145714235","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":"IL-2/IL-2Ab complexes expand regulatory T cells in vivo and provide neuroprotection after cardiac arrest","authors":"Shan Wu ,&nbsp;Xuanyu Chen ,&nbsp;XiaoMei Ling ,&nbsp;Yunyang Han ,&nbsp;Shaomei Chen ,&nbsp;Wei Wang","doi":"10.1016/j.imlet.2025.107113","DOIUrl":"10.1016/j.imlet.2025.107113","url":null,"abstract":"<div><div>Cardiac arrest (CA) results in global ischemia/reperfusion injury and severe neurological dysfunction, for which effective therapeutic interventions remain limited. Regulatory T cells (Tregs) play a crucial role in modulating post-ischemic inflammation and promoting neuroprotection. In this study, we demonstrate that in vivo expansion of Tregs using the interleukin-2/interleukin-2 antibody (IL-2/IL-2Ab) complex significantly increased Treg numbers in the blood, spleen, and lymph nodes. Mice pretreated with the IL-2/IL-2Ab complex before cardiac arrest and cardiopulmonary resuscitation (CA/CPR) exhibited improved neurological recovery, reduced ischemic brain injury, and enhanced survival rates. These findings highlight a potential immunomodulatory strategy for improving outcomes after cardiac arrest. The IL-2/IL-2Ab complex may represent a promising adjunctive therapy to attenuate post-resuscitation brain injury through the selective expansion of protective Tregs.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"278 ","pages":"Article 107113"},"PeriodicalIF":2.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145632996","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":"Lenvatinib-resistant liver cancer-derived HSP90α-containing extracellular vesicles enhance drug resistance via macrophage CXCL8 secretion","authors":"Xin-Wei Xu ,&nbsp;Yue Zhang ,&nbsp;Cheng-Wen Zhao ,&nbsp;Han Wu ,&nbsp;Meng-Ting Zhang ,&nbsp;Yu-Ting Ma ,&nbsp;Yang Yu ,&nbsp;Lu Zheng ,&nbsp;Feng Gu ,&nbsp;Yong-Qiang Chen","doi":"10.1016/j.imlet.2025.107122","DOIUrl":"10.1016/j.imlet.2025.107122","url":null,"abstract":"<div><div>The acquisition of lenvatinib resistance has a significant detrimental impact on the clinical efficacy of patients with hepatocellular carcinoma (HCC). Extracellular vesicles (EVs), which act as key mediators of intercellular communication, are implicated in tumor progression and immune evasion. The aim of this research was to investigate whether EVs derived from lenvatinib-resistant HCC cells regulate tumor-associated macrophages and contribute to drug resistance in HCC. The results showed that lenvatinib-resistant HCC cell-derived EVs could upregulate the ERK pathway in macrophages, leading to the secretion of C-X-C motif chemokine ligand 8 (CXCL8), which, in turn, promoted HCC cells resistant to lenvatinib. Mechanistically, lenvatinib-resistant HCC cell-derived EVs regulate the Toll Like Receptor 2 (TLR2)-ERK pathway in macrophages through heat shock protein 90 alpha (HSP90α), thereby promoting the secretion of CXCL8, and activating STAT3 phosphorylation, which in turn upregulates the expression of Programmed Cell Death Ligand 1 (PD-L1). Subsequently, elevated levels of CXCL8 stimulated the CXCL8 receptor CXC chemokine receptor 1/2 (CXCR1/2) in HCC cells, inhibited lenvatinib-induced apoptosis, and increased the expression of P-glycoprotein (P-gp) and Vimentin, thereby promoting epithelial-mesenchymal transition (EMT) and drug resistance in liver cancer. Conversely, the inhibition of CXCR1/2 abolished its inhibitory effect on lenvatinib-induced apoptosis, and resulted in the downregulation of P-gp and Vimentin. In conclusion, our study demonstrated that EVs containing HSP90α, derived from lenvatinib-resistant liver cancer cells, can promote EMT and drug resistance in HCC cells by stimulating CXCL8 secretion from macrophages. This finding may provide new insights and strategies to overcome lenvatinib resistance in the future.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"278 ","pages":"Article 107122"},"PeriodicalIF":2.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145687383","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":"Comparison of IgG antibody levels, avidity, and subclass distribution against pertussis toxin in children and adolescents after four-dose primary whole-cell (DTwP) or acellular (DTaP) vaccination, each followed by a single DTaP booster","authors":"Waldemar Rastawicki ,&nbsp;Aleksandra Anna Zasada","doi":"10.1016/j.imlet.2025.107115","DOIUrl":"10.1016/j.imlet.2025.107115","url":null,"abstract":"<div><div>Vaccination plays a key role in the prevention of pertussis, the infectious disease that is endemic worldwide. Two types of pertussis vaccines are currently in use: whole-cell (wP) and acellular (aP) vaccines. Differences in the duration of immunity have been observed depending on the vaccine type. In this study, the levels of individual IgG subclasses and antibody avidity were assessed in children vaccinated with either aP or wP vaccines. The results revealed no significant differences in the mean IgG antibody levels and avidity between children immunised with wP and those who received aP vaccines. However, in the vaccinated children IgG4 was a dominated IgG subclass, regardless of vaccine used (aP v. wP), whereas in pertussis patients the IgG1 was dominating. These findings need deeper investigation, in terms of a vaccine efficacy and wanning immunity, as typically in response to protein antigens IgG1 is dominating. Moreover, the observation of IgG4 predominance in vaccinated vs. IgG1 predominance in infected individuals might be a valuable parameter in pertussis diagnostics as it enables differentiation between infected and vaccinated but not-infected individuals.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"278 ","pages":"Article 107115"},"PeriodicalIF":2.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145623053","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":"TNFAIP8 targets ATG3 to regulate autophagy and participate in the molecular mechanism of ankylosing spondylitis","authors":"Yanyu Zhao ,&nbsp;Man Ni ,&nbsp;Hui Zhao ,&nbsp;Yuxin Ren ,&nbsp;Ziqi Li ,&nbsp;Hanqing Wu ,&nbsp;Longbao Xu ,&nbsp;Guoqing Li ,&nbsp;Faming Pan","doi":"10.1016/j.imlet.2025.107124","DOIUrl":"10.1016/j.imlet.2025.107124","url":null,"abstract":"<div><div>Ankylosing spondylitis (AS) is an immune-mediated inflammatory joint disease. This study aims to explore the molecular mechanism by which tumor necrosis factor alpha-induced protein 8 (TNFAIP8) regulates autophagy in AS. We collected 10 mL of peripheral venous blood from 48 patients with AS and 48 healthy controls, along with epidemiological data. The levels of inflammatory cytokines were measured using enzyme-linked immunosorbent assay (ELISA). Then, CD3+ <em>T</em> lymphocytes were isolated via magnetic bead sorting, and the transcriptional levels of TNFAIP8 and autophagy-related genes (ATG3, ATG5, ATG7, ATG12, Beclin1, and LC3B) were determined by real-time quantitative PCR (qRT-PCR). Using small interfering RNA (siRNA) technology, we knocked down TNFAIP8 expression in Jurkat T cells. Next, qRT-PCR and Western blot (WB) were used to detect the mRNA and protein levels of TNFAIP8 as well as the autophagy markers p53, TFEB, ATG3, p62, and LC3. Co-immunoprecipitation (Co-IP) assays confirmed the interaction between TNFAIP8 and ATG3. In T cells from AS patients, TNFAIP8 and ATG3 levels are down-regulated and positively correlated (<em>r_s</em> = 0.350, <em>P</em> = 0.015). Further experiments demonstrated that si-TNFAIP8 reduced the mRNA and protein levels of ATG3. Co-IP verified TNFAIP8 interacts with ATG3.TNFAIP8 may regulate AS autophagy by targeting ATG3.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"278 ","pages":"Article 107124"},"PeriodicalIF":2.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145804296","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}