392 papers
This study reveals that the alternative polyadenylation factor CFIm25 enhances macrophage antibacterial immunity against *Salmonella* by preventing 3' UTR lengthening of key targets like TAB2, thereby amplifying MAPK and NF-κB signaling to promote pro-inflammatory responses and suppress the immunosuppressive M2 state.
This study identifies GFI1 as a novel cell-intrinsic regulator that restricts the expansion of IL-17-producing γδT17 cells by directly repressing the transcription factor MAF, thereby controlling lineage commitment and the balance between IL-17 and IFNγ-producing γδ T cell subsets.
This study characterizes the longitudinal dynamics of CD4+ T cell and IgG responses following de novo yellow fever vaccination, revealing a peak in polyclonal T cell activation and antibody levels at 22–43 days followed by repertoire contraction and sustained, highly specific immunity one year later.
This study utilizes cryo-electron tomography to reveal the progressive ultrastructural collapse of the podocyte slit diaphragm, from initial membrane bending to eventual disappearance and cytoskeletal reorganization, thereby elucidating the structural mechanisms underlying anti-nephrin-mediated podocytopathy.
This study demonstrates that decidual macrophages in early-onset preeclampsia exhibit impaired efferocytosis and phagocytosis due to a failure to upregulate scavenger receptors, leading to the accumulation of apoptotic trophoblasts and a shift toward a pro-inflammatory phenotype characterized by increased CXCL-8 and IL-6 release.
This study presents a multi-scale mathematical model integrating BCR and TCR repertoire diversity to mechanistically explain immune imprinting, infection control dynamics, and cancer-immune interactions, thereby establishing a quantitative framework for optimizing vaccine schedules and immunotherapies.
This study reveals that circadian clock proteins CRY1 and CRY2 form oscillatory complexes with the NLRP3 inflammasome to act as a time-of-day-dependent checkpoint that restrains inflammatory activation, a mechanism whose disruption by disease-associated mutations alters both the timing of inflammation and drug responsiveness.
The novel PDE10A inhibitor ADT-030 suppresses tumor growth by disrupting MAPK signaling in both tumor cells and myeloid-derived suppressor cells to induce immunogenic cell death and reshape the tumor microenvironment, thereby unleashing a host-dependent antitumor immune response that synergizes with anti-PD-1 therapy.
This study reveals that *Drosophila melanogaster* larvae utilize taste receptors to detect bacterial peptidoglycans and trigger a non-canonical immune pathway that primes the cellular immune system, thereby enhancing survival against future infections.
This study utilizes immunopeptidomic analysis to characterize the distinct landscape of cross-presented glioblastoma antigens, revealing that APC-intrinsic processing limits tumor-specific epitope presentation and demonstrating that mRNA vaccines targeting these specific cross-presented antigens effectively delay tumor growth and elicit robust T cell responses.
This study demonstrates that regulatory T cells (Tregs) protect mucosal tissues from excessive damage by restraining IL-15-mediated bystander and cytotoxic CD8 T cell activity through the limitation of IL-2 and IL-15 trans-presentation, while preserving essential antigen-driven memory responses.
The study demonstrates that the combined steady-state expression levels of LynA and LynB isoforms, rather than their specific identity, determine a dose-dependent threshold for macrophage signaling by simultaneously activating both positive-regulatory Syk and negative-regulatory SHIP1, thereby capping downstream responses in the absence of receptor engagement.
This study utilizes whole-genome DNA methylation profiling of cerebrospinal fluid cells to reveal immune regulatory alterations in multiple sclerosis, highlighting a novel pathogenic role for protocadherin genes in T cell activation and migration.
This study utilizes mouse genetics to demonstrate that IKK-regulated inflammatory pathways play distinct, subset-specific roles in T cells, where IKK-dependent NF-B activation is essential for the development of type 1 cells but only for the long-term survival of adaptive cells, while IKK-mediated repression of RIPK1 is crucial for preventing necroptosis in peripheral T cells, collectively revealing a regulatory complexity that contrasts with T cell biology.
This study of 170 Azerbaijani children found that while SARS-CoV-2 infection significantly elevated IL-6 and IL-18 levels compared to healthy controls, vitamin D deficiency showed only a non-significant trend toward further increasing these inflammatory cytokines, suggesting a potential but unproven modulatory role for vitamin D in pediatric COVID-19 responses.
This study demonstrates that healthy individuals possess distinct autoreactome profiles determined by their HLA-DRB1 genotypes, suggesting that specific HLA alleles may predispose individuals to pathogenic autoantibodies even in the absence of overt autoimmune disease.
This study demonstrates that structural features derived from AI-predicted TCR-pMHC models, particularly those generated by AlphaFold2, are more effective than sequence-based features in distinguishing immune interactions, revealing that non-interacting complexes exhibit similar structures but lower energetic stability.
This study reveals that macrophages in cardiac allografts exhibit higher intracellular iron levels and SLC11A1 expression compared to those in tumors, and demonstrates that myeloid-specific deletion of Slc11a1 alleviates macrophage inflammation and cardiac allograft rejection, identifying SLC11A1 as a potential therapeutic target for regulating immune responses in both transplant and tumor contexts.
CARTiBASE is a freely available, interactive web platform that consolidates and standardizes over 10,000 Chimeric Antigen Receptor (CAR) sequences from diverse sources to enable efficient retrieval, comparative analysis, and exploration of design trends in cellular immunotherapy.
This paper introduces CALM, a contrastive learning-based dual-encoder architecture that treats antibody-antigen recognition as molecular translation to enable bidirectional sequence-to-specificity prediction, achieving a 7% top-1 retrieval rate on a rigorous, leakage-controlled test set.