The underlying proinflammatory mechanism of coagulation factor VⅡ in coronary artery disease (CAD) remains unclear. According to the inclusion criteria, 24 non-CAD subjects and 24 patients with CAD were enrolled. The expression levels of pro-inflammatory (CD14+CD86+, CD14+CD163-), anti-inflammatory monocytes (CD14+CD163+), CD14+CD142+ and CD14+PAR2+ monocytes in peripheral blood were detected by flow cytometry. The levels of TNF-α, IL-1β, IL-6, IL-10, and FVⅡ in plasma were determined by ELISA. In vitro experiments were conducted to induce inflammatory THP-1 by FVⅡa. The FVⅡa/TF complex inhibitor PCI-27,483 and PAR2 antagonist AZ3451 were used to clarify the mechanisms. Compared with the control group, the percentage of CD14+CD86+ pro-inflammatory monocytes were significantly increased in the CAD group, and further elevated after PCI. The results of the levels of CD14+CD142+ and CD14+PAR2+ monocytes showed the same trends with CD14+CD86+ pro-inflammatory monocytes. The levels of CD14+CD163+ anti-inflammatory monocytes and IL-10 were decreased in CAD patients, but increased after PCI. The pro-inflammatory factors and FVⅡ were significantly elevated in the CAD group and significantly decreased after PCI. Correlation analysis revealed that FVⅡ, TF, and PAR2 were significantly associated with CD14+CD86+ pro-inflammatory monocytes, and inflammatory factors. In vitro studies further confirmed that the FVⅡa/TF coagulation complex and PAR2 could activate NF-κB in monocytes and aggravate inflammation. Our findings suggest that crosstalk between monocytes and the coagulation complex might contribute to residual inflammation in CAD, potentially involving the FVIIa/TF/PAR2-NF-κB signaling pathway. Based on these observations, we hypothesize that blocking the interaction between clotting factors and monocytes could represent a promising therapeutic strategy to mitigate residual inflammation, but further rigorous experiments are needed for verification.

This study aims to investigate the prevalence, clinical characteristics, and prognostic significance of anti-neutrophil cytoplasmic antibodies (ANCA) across different subtypes of interstitial lung disease (ILD), specifically idiopathic pulmonary fibrosis (IPF), connective tissue disease-associated ILD (CTD-ILD) without ANCA-associated vasculitis (AAV), and AAV-ILD. A cross-sectional study was conducted to evaluate the positivity rate and clinical characteristics of ANCA in ILD. In the following meta-analysis, PubMed, Web of Science and Scopus were searched for eligible studies reporting positivity rate of ANCA in ILD. The pooled positivity rates of ANCA, MPO and PR3 in ILD were calculated, and survival outcome between ANCA-positive and ANCA-negative ILD patients were compared. Sensitivity analyses, subgroup analyses and meta-regression was also conducted. A total of 217 ILD patients were enrolled in this cross-sectional study, with an ANCA positivity rate of 7%. In the meta-analysis, with 24 studies and 4,424 patients, the pooled positivity rate of ANCA in IPF, CTD-ILD without AAV, and AAV-ILD were 9%, 15% and 97%, respectively. In patients with IPF, patients with ANCA positivity were more likely to develop honeycombing (OR 2.70, 95%CI 1.09, 6.70, p = 0.03). No significant difference was observed in survival time between IPF patients with or without ANCA positivity (HR 1.18, 95%CI 0.73, 1.90). The positivity rate of ANCA varies significantly across different subtypes of ILD. Future research should focus on the characteristics and prognostic value of ANCA positivity in other ILD subtypes.

To assess the effectiveness and safety of intravenous efgartigimod in patients with myasthenia gravis (MG) and to compare treatment responses between anti-acetylcholine receptor antibody (AChR-Ab)-positive and -negative subtypes. A comprehensive search was conducted in the PubMed, Scopus, Web of Science, and Cochrane CENTRAL databases up to 15 October 2025. Clinical trials and cohort studies evaluating the effectiveness and safety of efgartigimod in patients with MG were included. A random-effects model was used to pool mean differences (MDs) for continuous outcomes and proportions for categorical outcomes, with corresponding 95% confidence intervals (CIs). Subgroup analyses were performed based on study design and MG subtype. Twenty-nine studies (1594 patients) were included. Overall, 83% of patients achieved clinically meaningful improvement (CMI; ≥ 2-point reduction in MG Activities of Daily Living [MG-ADL] score), and 36% achieved minimal symptom expression (MSE; MG-ADL score of 0 or 1) with no significant difference between AChR-Ab-positive and AChR-Ab-negative subtypes. MG-ADL score significantly decreased from baseline (MD: -4.3 points, 95% CI: -4.99 to -3.61), with no difference between the MG subtypes. Quantitative MG score (QMG; MD: -3.6 points, 95% CI: -4.28 to -2.91), MG Quality of Life 15-item revised scale (MG-QoL15r), IgG levels, and corticosteroid use showed significant reductions in the AChR-Ab-positive subtype; however, these outcomes were not reported in the AChR-Ab-negative subtype. Serious adverse events were reported in 4.42% of patients. Efgartigimod significantly improved clinical symptoms and quality of life in patients with MG and may offer a steroid-sparing effect, with no significant differences observed between subtypes.

Traditional vaccine development faced significant hurdles, including lengthy timelines and high costs, which hindered rapid responses to pathogens. Although the emergence of AI offered transformative potential, the necessity for a fully integrated workflow was often overlooked in studies focusing on individual tools. This review addressed a critical gap by synthesizing AI technologies across the vaccine design process, focusing on the integrated workflow from antigen discovery to clinical translation. A systematic framework was required to connect disparate tools and ensure seamless transitions. Consequently, this study provided a comprehensive roadmap for pandemic preparedness and vaccine discovery. A systematic analysis based on the PRISMA framework (2015-2024) was conducted, and 19 landmark articles were reviewed.It was demonstrated that the paradigm shift from predictive to generative AI offered unprecedented opportunities for developing novel antigens and adjuvants with superior immunogenicity. Synthesis of the literature revealed rapid progress toward sophisticated deep learning. Transformer models and Protein Language Models emerged as dominant for epitope prediction, while AlphaFold2 became the standard for structural modeling. The advent of generative AI for de novo antigen design represented the leading edge of the discipline. Additionally, AI-enhanced molecular dynamics and digital twin simulations accelerated clinical validation and manufacturing scalability. The "Integrated AI Workflow for Vaccine Design and Development" was emphasized as a comprehensive system and a prerequisite for sustainable innovation. Overall, this analysis served as a strategic roadmap for utilizing AI as a transformative framework for next-generation vaccine discovery and pandemic preparedness.

The production of antibodies against viral structural proteins such as the spike (S) and the nucleocapsid (N) is a hallmark of SARS-CoV-2 infection. The N protein contains several immunogenic regions. In this work we analysed epitope specificity and avidity of anti-N antibodies in COVID-19 patients. Eighty-nine COVID-19 patients were recruited. IgG, IgA, IgM antibodies to recombinant N protein and to 6 different peptides containing predicted B epitopes were measured by ELISA. Antibody avidity was evaluated by chaotropic ELISA. Anti-N IgG, IgA, and IgM were detected in 59%, 41% and 30% respectively; in 11% cases anti-N IgG are the only antibodies present in COVID patients. IgG and IgA anti-N antibodies levels correlate with levels of IL-6 and inversely with PaO2/FiO2 ratio (p < 0,005). Anti-N IgG displayed medium avidity in 51% and high avidity in 49% COVID patients; anti-N avidity was negatively correlated with PaO2/FiO2 (p < 0,05). Median anti-N antibody levels were similar in discharged or deceased patients and antibody avidity was not correlated with outcome. Among peptides, N366-388 is the most frequently recognized by IgG, IgA and IgM antibodies followed by N380-400, bound by patients IgG and IgA but anti-N380-400 IgG display higher avidity than anti-N366-388 IgG. These results indicate that anti-N antibodies are characterized by medium-high avidity and preferentially bind the COOH-terminus of the nucleoprotein. Anti-N antibodies, especially directed towards specific epitopes, might be relevant for the course of the infection, and their induction might improve current vaccination strategies.

Intravenous immunoglobulin (IVIg) is the standard of care for the treatment of Kawasaki disease (KD) and should be administered within 10 days of the onset of fever. Management guidelines for children with KD who defervesce spontaneously are not clear. In this study, we analysed patients with KD diagnosed between 1994 and 2024 at our centre who had defervesced spontaneously, had normal acute-phase reactants, and underwent echocardiographic examination, and in whom IVIg had not been administered. We reviewed the records of patients with KD from January 1994 - December 2024. The diagnosis of KD was based on standard guidelines. Patients with KD were said to be in spontaneous defervescence when they remained afebrile for ≥ 48 h, had normal acute-phase reactants [C-reactive protein (CRP), Erythrocyte sedimentation rate (ESR)] and no coronary artery abnormalities (CAAs) on echocardiography at presentation, and when IVIg was not administered. Patients with spontaneous defervescence were subdivided into (i) early defervescence (Ed-KD), if the interval between onset of symptoms and defervescence was < 10 days, and (ii) late defervescence (Ld-KD), if the duration between onset of symptoms and defervescence was ≥ 10 days, respectively. Details of the clinical profile, laboratory investigations, and echocardiography findings were obtained from the records. Of the 1499 patients with KD enrolled during the study period, 115 patients (7.7%; 86 boys) defervesced spontaneously. The median age at disease onset was 6 years (mean, 5.6 years; range, 0.8-15 years). The median duration of fever, defined as the total duration of the febrile episode before spontaneous defervescence, was 5 days (range, 1-21 days). The median interval between illness onset (defined as fever onset) and diagnosis of KD was 15 days (range, 4-40 days), indicating that diagnosis was often made after fever had already subsided. The most common clinical feature was periungual desquamation, followed by rash, oral-mucosal changes, cervical lymphadenopathy, and conjunctival injection. Incomplete presentation was noted in 73.9% (n = 85/115) of patients. No patient has developed CAAs or other cardiac sequelae over a median follow-up of 9 months (range 2 months-156 months). The cumulative follow-up for the cohort was 235 patient-years. The 'low-risk' subgroup of patients with KD who defervesce spontaneously, and have normal acute phase reactants with no CAAs at presentation, have good clinical and coronary outcomes.

This article presents a case of recurrent autoimmune hemolytic anemia in a child with a gain-of-function (GOF) mutation of the TLR7. This patient's condition contrasts with the six previously documented cases of GOF mutations in the TLR7, thereby expanding the phenotypic spectrum of such mutations and enhancing clinical comprehension of childhood systemic lupus erythematosus (cSLE). The article discusses the mechanisms by which TLR7 GOF mutations can result in autoimmune hemolytic anemia, explores the influence of cytomegalovirus (CMV) infection on the disease's development and progression, and emphasizes the therapeutic potential of hematopoietic stem cell transplantation for cases of TLR7 GOF mutations.