377 papers
This study demonstrates that HIV-1 infection does not inherently protect CD4+ T cells from cytotoxic T lymphocyte-mediated killing, as observed survival advantages in actively infected cells are primarily due to Nef-dependent downregulation of MHC class I molecules rather than intrinsic resistance to cell death.
This study demonstrates that HDAC1 inhibition in myeloid-derived suppressor cells (MDSCs) upregulates the lncRNA Malat1 to suppress pSTAT3 signaling, thereby inducing apoptosis and cell cycle arrest while reducing the cells' ability to inhibit T cell proliferation.
This study demonstrates that a transient wave of neonatal regulatory T cells is essential for normal alveologenesis by restraining neutrophil-mediated inflammation, thereby preventing structural lung abnormalities and preserving epithelial balance.
A medium-chain triglyceride and omega-3 fatty acid-rich ketogenic diet accelerates blood-spinal cord barrier resealing and modulates immune cell populations to reduce inflammation and promote functional recovery in a preclinical model of multiple sclerosis.
This study utilizes multi-omics approaches to demonstrate that while healthy oral mucosa maintains neutrophils in discrete immunoregulatory states, periodontitis disrupts this balance by promoting blood-like infiltration and systemic reprogramming of circulating neutrophils, thereby linking localized tissue inflammation to broader inflammatory disease pathogenesis.
This study demonstrates that Hsa_circ_0000629 exacerbates bronchial asthma by acting as a molecular sponge for miR-212-5p, thereby upregulating NLRP3 expression and promoting inflammation and apoptosis, suggesting this axis as a potential therapeutic target.
This study identifies a distinct circulating pre-osteoclast population derived from classical monocytes that is expanded in active psoriatic arthritis, primed for osteoclast differentiation without exogenous RANKL, and actively recruited to inflamed synovial tissue, thereby elucidating the systemic immune mechanisms driving bone erosion in the disease.
This study reveals that a specific subset of monocyte-derived lung cells limits immunity to *Mycobacterium tuberculosis* due to impaired IFNγ signaling and type I IFN-mediated suppression, a mechanism that can be overcome by prior immunity to reduce bacterial burdens.
This study identifies the transcription factor Bhlhe40 as a critical, therapy-specific regulator of T cell effector differentiation and metabolic fitness that is essential for anti-PD-1 efficacy via CD8 T cells but dispensable for anti-CTLA-4 efficacy due to compensatory CD4 T cell mechanisms.
This study reveals how somatic hypermutation enables public IGHV1-69 antibodies to adapt to SARS-CoV-2 antigenic escape mutations and identifies an AI-discovered ultrapotent antibody, ZL525, that overcomes even the most evasive variants, including those with new glycosylation sites, while maintaining broad sarbecovirus neutralization.
This study demonstrates that *Salmonella* Typhi asparaginase depletes host asparagine to activate the mTOR-GCN2 integrated stress response in murine macrophages, a pathway essential for bacterial clearance and cytokine production that highlights key nutrient-sensing differences between restrictive murine and susceptible human hosts.
This study reveals that the innate immune system detects *Plasmodium* sporozoite traversal of host cells as a wounding event, a mechanism independent of inflammasome or Toll-like receptor signaling but dependent on T cells, which is essential for priming protective CD8+ T cell immunity.
This study utilizes single-cell transcriptomics to reveal that elevated frequencies of atypical B cells, characterized by specific markers and gene expression profiles, are a key determinant of both influenza vaccine non-responsiveness and severe infection outcomes.
This study demonstrates that the specific mode of programmed macrophage death critically determines cutaneous wound healing outcomes, where necroptosis disrupts tissue architecture and repair resolution, while enhanced apoptosis preserves tissue integrity and reduces scarring.
This study identifies that metabolic reprogramming of Th17 cells via the OXPHOS pathway drives LIGHT-mediated airway remodeling in severe mixed granulocytic asthma, demonstrating that dual blockade of OXPHOS and LIGHT effectively reverses disease features and restores regulatory T cell numbers.
This study reveals that heterozygous gain-of-function mutations in STAT1 drive autoimmunity by promoting the differentiation of T follicular helper type 1 cells and excessive IFN-γ production, a mechanism that can be therapeutically targeted by IFN-γ neutralization.
This study demonstrates that mixed hematopoietic chimerism in NOD mice restores immune tolerance by generating donor-derived CD8+CD122+ regulatory T cells that selectively eliminate autoreactive T cells through a perforin/granzyme-B-dependent mechanism, offering a potential therapeutic strategy for Type 1 diabetes given the observed deficiency of these cells in human patients.
This study demonstrates that ImmTACs can overcome cytotoxic T cell suppression by triggering calcium signaling and subcellular polarization to induce tumor cell cytolysis, even though they fail to elicit IFN-gamma secretion under these conditions.
This study demonstrates that osteopontin (OPN), produced by a specific neutrophil subtype during *Staphylococcus aureus* skin infections, is a critical mediator of tissue repair that accelerates lesion healing and reduces lesion size, suggesting its potential as a therapeutic target for improving infection resolution.
This study demonstrates that endotoxemia resulting from gut barrier dysfunction in colitis triggers anemia by activating TLR4 on CD169+ tissue-resident macrophages, a mechanism that can be mitigated by TLR4 inhibition to protect against both inflammation and anemia.