386 papers
Drosophila tracheal terminal cells maintain their essential Foxo-dependent structural plasticity and respiratory function by being immune privileged through the absence of PGRP-LC, which prevents lethal immune activation and cell death that would otherwise compromise their dynamic remodeling capabilities.
The long isoform of ZAP restricts viral replication by preferentially binding viral RNA and recruiting a specific cascade of enzymes (KHNYN, TUT4/TUT7, DIS3L2, and XRN1) to execute complete transcript decay, a process enhanced by TRIM25 during viral infection.
This study demonstrates that specific HLA alleles imprint distinct, germline-encoded biases on TCR Vβ segment usage through direct molecular contacts, establishing a biological prior that shapes the T cell repertoire independently of thymic selection or specific infections.
This study demonstrates that the pathogenic impact of MuSK autoantibodies in myasthenia gravis is determined by a complex interplay of antibody valency and epitope specificity, which differentially influence MuSK signaling kinetics, Dok7 binding, and gene expression without necessarily increasing receptor internalization.
This study identifies bone marrow-derived Trem2hi macrophages as critical mediators that bridge inflammation resolution and fibrosis initiation in ischemia-reperfusion kidney injury by promoting efferocytosis and regulating cholesterol metabolism, thereby suggesting them as a potential therapeutic target for preventing the progression from acute kidney injury to chronic kidney disease.
This study reveals that MAIT cells exhibit tissue- and activation-dependent polyfunctional responses to *Staphylococcus aureus*, where their susceptibility to the bacterial toxin HlgAB is modulated by their activation status and tissue origin, with tonsillar cells showing greater resistance than blood-derived cells.
This study characterizes the human monoclonal antibody 3A06, which achieves broad neutralization of dengue and Zika viruses by targeting a light chain-dominated quaternary epitope on viral E protein dimers, with its efficacy against all dengue serotypes further enhanced by IgG3 subclass switching that leverages the Fc-hinge's extended reach and flexibility.
This study demonstrates that systemic sclerosis-associated autoantibodies against human topoisomerase 1 can cross-react with structurally homologous topoisomerase 1 from fungi, providing functional evidence that microbial antigens may trigger and perpetuate B cell-mediated autoimmunity in this disease.
By integrating multi-omics spatial profiling with a novel single-cell transformer model across sequential lymph nodes from triple-negative breast cancer patients, this study maps critical immune alterations and communication deficits during metastasis, identifying MARCO+ macrophages and CD1c+ cDC2 preservation as key biomarkers for prognosis and immunotherapy response.
This study demonstrates that a structure-guided computational approach successfully deimmunized the major cat allergen Fel d 1 by introducing specific mutations like K29G, which significantly reduced IgE reactivity and basophil activation while preserving cellular function, thereby offering a promising strategy for safer immunotherapies and the development of hypoallergenic cats.
This study demonstrates that an immunopeptidomics-guided approach, which integrates whole exome sequencing, transcriptomics, and mass spectrometry to filter neoantigens based on observed HLA peptide presentation, significantly improves the success rate of identifying functional neoantigens for personalized cancer vaccines in non-small cell lung cancer patients.
This study utilizes Hi-C technology to demonstrate that alcohol-associated hepatitis alters the 3D chromatin architecture of monocytes, specifically disrupting the genomic structure around clustered innate immune genes and thereby driving their dysregulated proinflammatory expression.
This study demonstrates that type I and III interferons synergize with TNF to induce RIPK1-dependent intestinal epithelial cell death, a process exacerbated by ATG16L1 deficiency and linked to the pathogenesis of Crohn's disease and severe viral infections like COVID-19.
This study reveals that chronic hepatitis B virus infection induces CD4 T-cell senescence characterized by DNA damage and telomere erosion, while the concurrent activation of the MRN-ATM pathway acts as a compensatory mechanism to preserve T-cell function and regulate inflammation, offering potential therapeutic targets for HBV persistence.
This study reveals that aging-associated endo-lysosomal dysfunction, exacerbated by LRRK2 mutations, triggers a systemic STING-dependent inflammatory cascade via cytosolic self-DNA accumulation and extracellular vesicle shedding, which ultimately compromises the blood-brain barrier and drives neurodegeneration.
This study reveals that bone marrow erythroblasts produce specialized pro-resolving mediators, particularly Resolvin D5n-3 DPA via the enzyme Alox15, which instruct macrophage-mediated neutrophil development to ensure balanced effector functions and effective host defense against infection and inflammation.
This study demonstrates that miR-378a-3p, which is upregulated in atopic dermatitis lesions by IL-4 and *Staphylococcus aureus*, acts as a positive regulator of keratinocyte inflammatory responses by enhancing canonical NF-κB pathway activity and amplifying innate immune cytokine secretion, thereby potentially contributing to disease exacerbation.
This study demonstrates that using unpaired TCR and TCR sequences for training machine learning models significantly reduces sequencing costs while maintaining prediction accuracy and outperforming existing methods on unseen epitopes.
This study demonstrates that autophagy impairment via ATG4B deficiency alleviates experimental hypersensitivity pneumonitis severity by suppressing key inflammatory pathways, reducing immune cell recruitment, and inhibiting granuloma formation, thereby identifying autophagy as a critical driver of the disease and a potential therapeutic target.
This study identifies maternal neutrophils as a critical survival niche for *Listeria monocytogenes* that facilitates the bacterium's entry into placental trophoblast cells, thereby driving severe fetal infection.