@article{pmid40036077,

title = {Boosting effect of high-dose influenza vaccination on innate immunity among elderly: a randomized-control trial},

author = {Olivia Bonduelle and Tristan Delory and Isabelle Franco Moscardini and Marion Ghidi and Selma Bennacer and Michele Wokam and Mathieu Lenormand and Melissa Petrier and Olivier Rogeaux and Simon de Bernard and Karine Alves and Julien Nourikyan and Bruno Lina and Behazine Combadiere and Cécile Janssen},

doi = {10.1172/jci.insight.184128},

issn = {2379-3708},

year  = {2025},

date = {2025-03-01},

urldate = {2025-03-01},

journal = {JCI Insight},

abstract = {BACKGROUND: The high-dose quadrivalent influenza vaccine (QIV-HD) showed superior efficacy against laboratory-confirmed illness than the standard-dose quadrivalent influenza vaccine (QIV-SD) in randomized-controlled trials with elderly. However, specific underlying mechanism remains unclear.nnMETHODS: This Phase-IV randomized control trial compared early innate responses induced by QIV-HD and QIV-SD in 59 subjects aged >65 years. Systemic innate cells and gene signatures at Day (D) 0 and D1, hemagglutinin inhibition antibody (HIA) titers at D0 and D21 post-vaccination were assessed.nnRESULTS: QIV-HD elicited robust humoral response with significantly higher antibody titers and seroconversion rates than QIV-SD. At D1 post-vaccination, QIV-HD recipients showed significant reduction in innate cells, including conventional dendritic cells and natural killer cells than QIV-SD, correlating with significantly increased HIA titers at D21. Blood transcriptomic analysis revealed greater amplitude of gene expression in QIV-HD arm, encompassing genes related to innate immune response, interferons, and antigen processing and presentation and correlated with humoral responses. Interestingly, comparative analysis with a literature dataset from young adults vaccinated with influenza standard-dose vaccine highlighted strong similarities in gene expression patterns and biological pathways with the elderly vaccinated with QIV-HD.nnCONCLUSION: QIV-HD induces higher HIA titers than QIV-SD, a youthful boost of the innate gene expression significantly associated with high HIA titers.nnTRIAL REGISTRATION: EudraCT Number: 2021-004573-32.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39204272,

title = {BacSPaD: A Robust Bacterial Strains' Pathogenicity Resource Based on Integrated and Curated Genomic Metadata},

author = {Sara Ribeiro and Guillaume Chaumet and Karine Alves and Julien Nourikyan and Lei Shi and Jean-Pierre Lavergne and Ivan Mijakovic and Simon de Bernard and Laurent Buffat},

doi = {10.3390/pathogens13080672},

issn = {2076-0817},

year  = {2024},

date = {2024-08-01},

urldate = {2024-08-01},

journal = {Pathogens},

volume = {13},

number = {8},

abstract = {The vast array of omics data in microbiology presents significant opportunities for studying bacterial pathogenesis and creating computational tools for predicting pathogenic potential. However, the field lacks a comprehensive, curated resource that catalogs bacterial strains and their ability to cause human infections. Current methods for identifying pathogenicity determinants often introduce biases and miss critical aspects of bacterial pathogenesis. In response to this gap, we introduce BacSPaD (Bacterial Strains' Pathogenicity Database), a thoroughly curated database focusing on pathogenicity annotations for a wide range of high-quality, complete bacterial genomes. Our rule-based annotation workflow combines metadata from trusted sources with automated keyword matching, extensive manual curation, and detailed literature review. Our analysis classified 5502 genomes as pathogenic to humans (HP) and 490 as non-pathogenic to humans (NHP), encompassing 532 species, 193 genera, and 96 families. Statistical analysis demonstrated a significant but moderate correlation between virulence factors and HP classification, highlighting the complexity of bacterial pathogenicity and the need for ongoing research. This resource is poised to enhance our understanding of bacterial pathogenicity mechanisms and aid in the development of predictive models. To improve accessibility and provide key visualization statistics, we developed a user-friendly web interface.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38510150,

title = {Exogenous IL-2 delays memory precursors generation and is essential for enhancing memory cells effector functions},

author = {Shaoying Wang and Margaux Prieux and Simon de Bernard and Maxence Dubois and Daphne Laubreton and Sophia Djebali and Manon Zala and Christophe Arpin and Laurent Genestier and Yann Leverrier and Olivier Gandrillon and Fabien Crauste and Wenzheng Jiang and Jacqueline Marvel},

doi = {10.1016/j.isci.2024.109411},

issn = {2589-0042},

year  = {2024},

date = {2024-04-01},

urldate = {2024-04-01},

journal = {iScience},

volume = {27},

number = {4},

pages = {109411},

abstract = {To investigate the impact of paracrine IL-2 signals on memory precursor (MP) cell differentiation, we activated CD8 T cell  in the presence or absence of exogenous IL-2 (ex-IL-2). We assessed memory differentiation by transferring these cells into virus-infected mice. Both conditions generated CD8 T cells that participate in the ongoing response and gave rise to similar memory cells. Nevertheless, when transferred into a naive host, T cells activated with ex-IL-2 generated a higher frequency of memory cells displaying increased functional memory traits. Single-cell RNA-seq analysis indicated that without ex-IL-2, cells rapidly acquire an MP signature, while in its presence they adopted an effector signature. This was confirmed at the protein level and in a functional assay. Overall, ex-IL-2 delays the transition into MP cells, allowing the acquisition of effector functions that become imprinted in their progeny. These findings may help to optimize the generation of therapeutic T cells.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}