392 papers
This study identifies elevated CaMKK2 expression as a prognostic biomarker for biologically aggressive chronic lymphocytic leukemia (CLL) and demonstrates that inhibiting CaMKK2 reduces leukemic cell survival and disrupts supportive nurse-like cell interactions, highlighting its potential as a therapeutic target for high-risk patients.
This study reveals that high tumor glycolysis drives aberrant angiogenesis and T-cell exclusion to limit immunotherapy efficacy, but combining anti-angiogenic agents with immune checkpoint blockade can normalize the vasculature and restore CD8+ T cell recirculation, thereby overcoming resistance specifically in glycolysis-high tumors.
This study integrates multiomics analysis and CRISPR screening to map functional noncanonical translation events in the mouse immune system, revealing that thousands of previously uncharacterized coding sequences, including endogenous retroviral-derived proteins, play critical roles in macrophage viability and innate immune signaling.
This study demonstrates that an intranasally administered engineered sACE2-Fc decoy (B5-D3) confers complete prophylactic protection against SARS-CoV-2 in mice by redirecting virus-decoy complexes to airway phagocytes for Fc-dependent lysosomal degradation, thereby establishing a distinct antiviral mechanism that overcomes the limitations of current vaccines and therapies.
This study identifies a vagus nerve-spleen-retina axis in which the decline of vagal signaling reprograms splenic monocytes to become pro-inflammatory and migrate to the retina, thereby driving inflammation and increasing susceptibility to age-related macular degeneration.
This study introduces a scalable, perturbation-based framework that maps the NFκB signaling architecture in T-cells using functional outputs rather than direct phosphorylation measurements, successfully identifying novel negative regulators like TRRAP and CTDSPL2 that enhance T-cell cytotoxicity and cytokine production when disrupted.
This study elucidates the structural and biochemical mechanisms by which the promiscuous chicken MHC class I molecule BF2*21:01 balances a broad peptide repertoire with specific stability preferences, revealing simplifying principles that govern its anchor residue co-variation and offer a foundation for predicting pathogen peptides.
This study demonstrates that the magnitude of the secondary B cell response following SARS-CoV-2 mRNA booster vaccination is primarily constrained by pre-existing antibody feedback inhibition rather than being determined by the number of pre-existing memory B cells.
This study demonstrates that T cell receptor repertoire diversity, rather than epigenetic clocks, effectively distinguishes healthy elderly from frail individuals by revealing a CMV-driven shift in immune control from CD4+ to CD8+ T cells that correlates with frailty.
This study reveals that during *Pseudomonas aeruginosa* and *Aspergillus fumigatus* co-infection in cystic fibrosis patients, a complement-inflammasome signaling axis—where bacterial priming enhances macrophage C3 expression and fungal engagement of C3 receptors amplifies SYK/ERK-driven NLRP3 inflammasome activation—drives pathological IL-1 release and lung inflammation.
This study demonstrates that alpha-1-antitrypsin (AAT) enhances host defense against *Mycobacterium intracellulare* by binding to the glucocorticoid receptor to differentially regulate cytokine expression, specifically inhibiting infection-induced M-CSF while promoting GM-CSF, thereby skewing macrophages toward a phenotype more effective at controlling mycobacterial burden.
This study demonstrates that mucosal intratracheal BCG vaccination in mice uniquely reprograms interstitial macrophages and establishes spatially organized immune hubs with CD4 T cells, resulting in superior protection against tuberculosis compared to intravenous or subcutaneous routes.
VDJdive and ECLIPSE are computational methods that utilize an expectation-maximization algorithm to resolve ambiguous clonotypes in single-cell TCR sequencing data caused by chain dropouts or artifacts, thereby enhancing clone size accuracy and improving the tracking of T cell clones across biological conditions.
This study presents a scalable, ELISA-based pulldown method using 3M MgCl2 elution to isolate functional, antigen-specific antibodies from serum while preserving their neutralizing activity, enabling epitope-level resolution of immune responses such as distinguishing head- versus stem-targeting antibodies against influenza.
This study reveals that homotypic SLAMF1:SLAMF1 interactions between innate T cells and neutrophils trigger the release of soluble factors that activate neutrophils to effectively kill the fungal pathogen *Blastomyces dermatitidis*.
This study demonstrates that in the NOD mouse model of type 1 diabetes, ERAP deficiency paradoxically protects against the disease by altering T cell differentiation and epitope presentation, despite increasing the display of a key self-antigen, thereby highlighting the complex risks of therapeutically modulating ERAP activity in autoimmunity.
This study reveals that Reg3β promotes cardiac repair after myocardial infarction by selectively binding to aged neutrophils via paucimannosylated proteins, triggering their lysosome-mediated death and subsequent clearance by macrophages to resolve inflammation.
This study utilizes spatial transcriptomics to demonstrate that the CCL19-CCR7 axis is a key mediator of T cell recruitment in the leishmanin skin test, providing critical biomarkers to support the development and deployment of leishmanin antigens for disease surveillance and vaccine efficacy assessment.
This study utilizes a genetic knockout mouse model and spatial transcriptomics to demonstrate that host- and tumor-derived Osteopontin play distinct yet cooperative roles in colorectal cancer liver metastasis by driving tumor proliferation, modulating macrophage polarization, and suppressing T cells, thereby identifying OPN blockade as a promising therapeutic strategy.
This study presents a universal CRISPR-based platform that selectively eliminates endogenous TCRα and TCRβ chains to enhance the expression, pairing fidelity, and therapeutic potency of transgenic TCRs while preventing off-target autoreactivity and graft-versus-host disease, thereby advancing both cancer immunotherapy and autoimmune disease modeling.