374 papers
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.
Although IL-10 deficiency enhances early control of *Plasmodium yoelii* infection, this protective effect is independent of the expected increases in IFN-γ and IL-12, as well as the humoral response, indicating that IL-10 suppresses other distinct host-protective pathways.
This study reveals that pluripotency factors (NANOG, SOX2, OCT4) maintain antiviral resistance in human embryonic stem cells by constitutively expressing negative regulators like SOCS1, which suppress canonical interferon signaling to preserve the pluripotent state.
This study utilizes a human 3D microphysiological model to demonstrate that lymphatic endothelial cells actively regulate neutrophil migration and function during skin infection, revealing distinct, bacteria-specific responses to *Escherichia coli* and *Staphylococcus aureus*.
This study demonstrates that 5-Azacytidine enhances anti-leukemic immunity in myeloid malignancies by epigenetically reprogramming the myeloid niche to drive an S100A8/A9-mediated inflammatory cascade that licenses the functionality of immature NK cells, a mechanism supported by both preclinical models and clinical cohort data.
This study demonstrates that engineered bivalent bispecific CD28 antibodies (BiCos) effectively reverse T-cell anergy and quiescence induced by CD3-engaging bispecific T-cell engagers (TCEs) by restoring costimulatory signaling, thereby potently enhancing antitumor immunity and enabling tumor elimination even at low TCE doses.
This study demonstrates that the protein tyrosine phosphatase CD45 is essential for regulating polymorphonuclear neutrophil (PMN) trafficking, antimicrobial functions, and colonic mucosal repair through a CD11b-Lyn signaling axis, suggesting its potential as a therapeutic target for modulating PMN activity in inflammatory bowel disease.
This study demonstrates that the glucose transporter GLUT3 is non-redundantly essential for regulatory T cell metabolic fitness and suppressive function, as its specific deletion leads to severe autoimmunity, thereby challenging the prevailing view that Treg cells operate independently of glucose metabolism.
This study reveals that affinity maturation in a glycan-dependent HIV-1 antibody lineage enhances antigen recognition not by stabilizing the final bound state, but by leveraging somatic-germline residue synergy to reshape encounter state pathways, thereby increasing association rates and expanding the productive collision surface area.
By utilizing prefusion-stabilized HSV-2 glycoprotein B and LIBRA-seq technology, researchers identified four novel human antibodies that bind unique epitopes and provide potent cross-neutralization and protection against neonatal HSV-2 infection in mice.
This study demonstrates that clonal hematopoiesis of indeterminate potential (CHIP) acts as a systemic regulator that instructs maladaptive tissue repair and promotes fibrosis by reprogramming macrophages to drive inflammatory and profibrotic remodeling, thereby linking somatic evolution in blood cells directly to organ dysfunction.
This study demonstrates that ocrelizumab treatment in multiple sclerosis not only depletes B cells but also modulates T cell populations and enriches anergic, regulatory B cell subsets with enhanced IL-10 signaling and tissue-homing capabilities, thereby establishing a self-reinforcing regulatory immune circuit.
This study identifies Th17-derived miR-721 as a key driver of autoimmune myocarditis that promotes disease progression by repressing PPARγ to enhance Th17 responses, thereby establishing it as a promising therapeutic target for improving cardiac function.
This study demonstrates that glucocorticoid signaling directly upregulates the expression of the IL-27 subunit EBI3 in neonatal macrophages via nuclear translocation of the glucocorticoid receptor, suggesting that antenatal corticosteroid therapy may inadvertently increase immunosuppressive IL-27 levels and compromise survival during neonatal sepsis.
*Leishmania major* exploits a fibroblast-derived IL-7 feedback loop triggered by IFN-γ to induce an immunosuppressive monocyte subset that dampens CD4⁺ T-cell immunity and perpetuates infection.
This study reveals that mouse and human embryonic stem cells utilize an interferon-independent innate immune pathway where the RNA helicase Dhx9 stabilizes p53 and Stat1 to drive an interferon-stimulated gene response against dsRNA and viral infections like ZIKV.
This study demonstrates that autophagy significantly shapes the peptide repertoire presented by the rheumatoid arthritis-associated HLA-DRB1*04:01 allele by delivering endogenous autoantigens, particularly those related to ER stress, to MHC class II molecules, thereby potentially contributing to the breakdown of peripheral tolerance in rheumatoid arthritis.