258 papers
Immunology explores the intricate defense systems that keep our bodies safe from infections and disease. This field examines how our immune cells recognize threats, coordinate responses, and maintain a delicate balance between fighting invaders and avoiding self-harm. From understanding vaccine mechanisms to investigating autoimmune disorders, these studies reveal the dynamic biology protecting human health every day.
On Gist.Science, we ensure these critical discoveries remain accessible to everyone. We automatically process every new preprint in this category as it appears on bioRxiv, transforming complex research into both plain-language explanations and detailed technical summaries. This approach allows readers to grasp the core findings without getting lost in dense jargon, while still providing the depth needed for scientific inquiry.
Below are the latest immunology papers from bioRxiv, each accompanied by our curated summaries to help you navigate the newest breakthroughs in the field.
This study demonstrates that antigen-specific stimulation can reactivate HIV-1 proviruses integrated into transcriptionally repressive chromatin regions, indicating that these "deeply latent" reservoirs can contribute to viral rebound despite their epigenetic constraints.
This study characterizes the immune dysregulation in endometriosis by revealing elevated pathogenic Th17 cells and extensive transcriptomic reprogramming in Th17 subsets, suggesting that IL-23 and IL-17 targeted therapies could be repurposed to treat the disease.
This study utilizes high-throughput single-cell mass cytometry to demonstrate that cell cycle dynamics, particularly G1/S crosstalk with receptor signaling and S-G2 phase arrest, fundamentally shape human T cell fate and drive exhaustion programs in the context of cancer and CAR T cell therapy.
Through diverse infection models including ultra-low dose challenges, immune priming via co-housing, and pre-infection with Legionella pneumophila, this study demonstrates that Mycobacterium tuberculosis exhibits robust resistance to innate immune clearance regardless of the initial infectious dose or the strength of pre-existing innate inflammatory responses.
This study demonstrates that strong, sustained type I interferon signaling acts cell intrinsically to impair IFN responses in infected macrophages, thereby driving tuberculosis susceptibility, a process that can be reversed by genetically eliminating the positive regulator RESIST to restore IFN signaling and rescue host defense.
This study reveals that TCR signaling induces Id3 to reprogram potentially pathogenic V{gamma}1.1V{delta}6.3 {gamma}{delta} T cells into ILC1-like cells, a critical feedback mechanism that prevents severe autoimmunity resembling Sjogren's disease.
BenchRep-T is a unified benchmark that systematically evaluates nine computational approaches for T-cell receptor repertoire-based disease diagnostics, revealing that simple baselines often rival complex methods and highlighting the need for standardized, reproducible evaluation frameworks.
This study identifies TREM2 as a DAP12-associated receptor that directly binds to *Cryptococcus neoformans* via its -1,6-glucan cell wall component, thereby inhibiting macrophage phagocytosis and M1 polarization to suppress the host's antifungal immune response.
This study reveals that RA-associated oral bacteria induce neutrophil extracellular traps to generate citrullinated antigens, which are cross-presented by dendritic cells and autoreactive B cells to activate and expand cytotoxic CD8+ T cells via TLR signaling and IL-8 recruitment, thereby driving joint destruction in rheumatoid arthritis.
This study demonstrates that AlphaFold 3 can accurately predict the structures of MHC:peptide:TCR complexes, enabling a generalized model to decode T cell receptor antigen specificity for unseen epitopes with high accuracy.