388 papers
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.
Despite being upregulated during activation and inducing subtle mitochondrial ultrastructural changes, the metalloprotease YME1L1 is dispensable for T cell development, homeostasis, and acute activation, highlighting cell type-specific redundancies in mitochondrial quality control.
This study characterizes the functional divergence between regulatory (Nreg) and conventional (Nconv) bovine neutrophils during *Mycobacterium bovis* infection, revealing that while both subsets kill the pathogen, Nreg cells exhibit distinct transcriptional profiles, enhanced phagocytosis and ROS production, and unique mitochondrial and ultrastructural features that underscore a new layer of complexity in bovine tuberculosis pathophysiology.
This study reveals that inorganic pyrophosphatase-1 (PPa1) insufficiency causes a bone marrow-specific lysosomal storage disease characterized by the accumulation of glycolipids and the expansion of inflammatory macrophages, leading to impaired hematopoiesis and defective skeletal mineralization.
This study demonstrates that CSF1R-dependent macrophages in chickens, which exhibit distinct transcriptional profiles and functions compared to their mammalian counterparts, are essential for maintaining B cell development and preventing severe immune deficiency.
This study demonstrates that engineering T cells to target the 9G4 idiotope, a shared feature of pathogenic B cell receptors encoded by the IGHV4-34 gene, enables the precise elimination of autoreactive B cells in systemic lupus erythematosus and related diseases while preserving protective immunity and minimizing toxicity compared to conventional CAR-T therapies.
This study reveals that the immune system's coherent organization is encoded in a shared, multi-dimensional "immune transcriptional landscape" where coordinated gene expression deviations across diverse cell types align to define both dynamic shifts and stable, donor-specific structures.
The study demonstrates that low concentrations of DMSO, commonly used as a cryoprotectant or solvent, dose-dependently skew the in vitro differentiation of human T cells toward a memory phenotype, thereby potentially enhancing their efficacy for adoptive cancer immunotherapies.
This cross-sectional study demonstrates that in children with oligoarticular and polyarticular juvenile idiopathic arthritis, pain severity is independently associated with both systemic C-reactive protein levels and local synovial fluid markers of inflammation, particularly HMGB1.
This study demonstrates that systemic juvenile idiopathic arthritis is associated with hippocampal neuroinflammation and persistent alterations in peripheral neurobiological protein profiles driven by IL-6 and IL-18, identifying HMOX2 as a promising plasma biomarker for these central nervous system changes.
This study demonstrates that epidermal overexpression of CD109 attenuates cutaneous inflammatory responses in a psoriasis-like model by suppressing key inflammatory signaling pathways and reducing immune cell recruitment, suggesting its potential as a therapeutic target for inflammatory skin diseases.
By integrating genotyping and gene expression profiling of tonsil-derived immune cells from 103 children, this study identifies thousands of novel cell-type-specific eQTLs and eGenes, thereby expanding the genetic understanding of childhood atopic diseases and highlighting the importance of studying native tissues across human development.
This study reveals that IgG drives atherosclerosis by noncanonically activating macrophages as an endogenous TLR4 ligand, independent of antigen binding, which triggers inflammatory signaling and foam cell formation via the FcRn receptor.
This study demonstrates that the HEPLISAV-B vaccine effectively breaks immune tolerance and induces functional cure-like control of chronic hepatitis B in a mouse model through a CD4 T cell-dependent, non-cytolytic mechanism involving the CD40/CD40L signaling pathway.
This study reveals that CD8⁺ T cells induce interstrand crosslinking-associated DNA damage in neurons through non-contact mechanisms, suggesting that this genotoxic effect contributes to the neuronal dysfunction observed in viral infections and various neurodegenerative diseases.
This study reveals that despite diverse lung insults, monocyte-derived alveolar macrophages follow a conserved, hard-wired differentiation blueprint involving EGR2-mediated rewiring that establishes a stereotypical, protective phenotype, whereas fetal-derived macrophages exhibit more context-dependent plasticity.
This study reveals that age dictates NK cell fate and tissue distribution during CMV infection, showing that infant NK cells develop distinct adaptive-like responses and seed tissues to compensate for limited T cell immunity, whereas adult responses are shaped by competition with memory T cells.
This study demonstrates that autoantibodies against the epithelial integrin αvβ6, which are specific biomarkers for ulcerative colitis, actively inhibit mucosal TGFβ activation, disrupt epithelial homeostasis, and increase susceptibility to intestinal inflammation.
This study demonstrates that knocking down the long isoform of the prolactin receptor (LFPRLR) using a splice-modulating oligomer selectively targets pathogenic immune cells, reduces type I interferon signaling and autoreactive antibodies, and prevents lupus nephritis in SLE-prone mice without harming healthy immune cells, offering a promising new therapeutic strategy for systemic lupus erythematosus.