370 papers
This study demonstrates that time-restricted feeding alleviates allergic dermatitis in mice by modulating leptin-driven inflammatory pathways, offering a potential therapeutic strategy for inflammatory skin diseases without requiring caloric restriction.
This study demonstrates that Lineage 2-Beijing *Mycobacterium tuberculosis* strains evade BCG-induced trained innate immunity by suppressing key macrophage activation pathways, leading to impaired bacterial control both in vitro and in human contacts.
This study reveals that while CD31+ T-cells (angiogenic T-cells) inherently express higher levels of VEGF-A and CXCR4 than their CD31- counterparts, advancing age is associated with a pathological shift characterized by a reduced proportion of CD4+ T-cells but significantly elevated VEGF-A expression within the remaining T-cells, suggesting a potential link to age-related inflammation.
This study reveals that *Staphylococcus aureus* biofilms impair macrophage immune responses by reducing cGAS expression rather than degrading signaling molecules, and demonstrates that directly activating STING with 2'3'-cGAMP bypasses this defect to restore interferon responses, offering a promising therapeutic strategy for chronic implant-related infections.
This study provides the first integrated multiomic profile of extracellular vesicles from wild-type EBV-transformed B-cells, revealing that they export abundant host DNA and the viral lncRNA EBER1 while containing minimal viral DNA, thereby suggesting a vesicle-mediated mechanism for delivering viral RNA to distal tissues like the CNS in multiple sclerosis.
This study establishes that T-bet-expressing B cells are a specialized subset essential for generating protective mucosal and systemic antibody responses against murine norovirus infection, driving effective germinal center reactions and viral clearance.
This study identifies neutrophils as the earliest immune cells capable of detecting and surveilling preneoplastic breast cancer epithelial cells through the unfolded protein response, thereby establishing their critical role in the initial stages of tumor immunosurveillance.
This study demonstrates that the *Staphylococcus aureus* serine protease-like protein B (SplB) acts as a potent allergen capable of inducing severe eosinophilic airway inflammation and asthma-like symptoms in mice through a mechanism dependent on its enzymatic activity, the host's adaptive immune system, and the soluble protease sensor IL-33.
Cipolla et al. demonstrate that pre-existing antibodies enhance germinal center and plasmablast responses through Fc gamma receptor-dependent mechanisms while simultaneously lowering the affinity threshold for B cell entry via Fc gamma receptor- and complement receptor-independent pathways.
This study demonstrates that intestinal epithelial cells presenting bacterial antigens injected via the type 3 secretion system are essential for driving robust CD4 T cell responses and programming tissue-resident memory, highlighting a critical role for non-professional antigen presentation in mucosal immunity and vaccine development.
This study demonstrates that spontaneous pregravid obesity in rhesus macaques fundamentally reshapes fetal immune ontogeny by inducing tissue-specific reprogramming of innate and adaptive cells, characterized by heightened inflammation, impaired differentiation, and disrupted cell-cell communication, which provides a mechanistic basis for the increased susceptibility to immune-related diseases in offspring.
This study introduces the Quantitative Extrapolation from Single-tags (QuEST) immunofluorescence microscopy method to calibrate fluorescence signals against molecular copy numbers, revealing a 1:1 ZAP-70:TCR stoichiometry in human primary T cells and demonstrating that PD-1 engagement disrupts intrinsic CD28 recruitment during TCR activation.
This study establishes novel type I and type III interferon receptor knockout chicken models to demonstrate that type I interferon is critical for innate and adaptive immune regulation, while both interferon types play strain-specific roles in orchestrating pathogenesis and tissue tropism during avian influenza infection.
This study demonstrates that an optimized multiple amplification protocol successfully generates highly pure, potent, and metabolically stable allogeneic human Vγ9Vδ2 T cells with a Th1-like effector memory phenotype, supporting their development as a scalable, off-the-shelf platform for adoptive cell transfer immunotherapy.
This study identifies glutaminolysis as a critical metabolic dependency in emergency myelopoiesis driven by Myc, demonstrating that targeting this pathway pharmacologically or genetically can selectively suppress pathological myeloid overproduction and inhibit breast tumor progression without compromising normal hematopoiesis.
This study identifies a conserved metabolic-oxidative axis, driven by activation-induced glucose utilization and ROS production, as the primary cause of immune cell cryo-vulnerability and demonstrates that targeting this pathway with metabolic inhibitors and antioxidants can significantly restore post-thaw viability and antitumor efficacy across multiple immune cell types.
This study reveals that porcine STING stability and antiviral signaling are species-specifically regulated by RNF5-mediated K48-linked ubiquitination at lysine 61, which targets the protein for proteasomal degradation, a process counteracted by the deubiquitinase USP20 to enhance antiviral immunity.
This study demonstrates that mRNA vaccines targeting the malaria merozoite surface protein PfMSP2, particularly in a bivalent format, induce robust, multifunctional antibody responses comparable to or superior to recombinant protein vaccines, offering a promising strategy for next-generation malaria eradication.
This study utilizes multimodal immune profiling to reveal that CFTR dysfunction drives a spectrum of systemic immune dysregulation, demonstrating that even healthy F508del carriers exhibit a low-grade inflammatory signature similar to cystic fibrosis patients, thereby challenging the traditional binary distinction between health and disease.
The study demonstrates that the signaling molecule D-β-hydroxybutyrate enhances mitochondrial ATP production via oxidative phosphorylation, which suppresses stress responses and promotes chromatin accessibility at effector gene loci to drive CD8+ T cell differentiation and potent antitumor immunity.