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.
The paper introduces replicateFest, an R package and Shiny web application designed to analyze T cell receptor repertoire data from Functional Expansion of Specific T cell (FEST) assays by employing statistical models that account for biological and technical replicates to robustly identify antigen-specific clonotypes.
This study demonstrates that distinct melanoma-derived extracellular vesicle subpopulations, specifically gp100 and GPNMB, differentially reflect immune and stress-induced tumor states, offering a clinically feasible, non-invasive blood-based approach to monitor tumor burden and immune dynamics without prior vesicle isolation.
This study demonstrates that while isolated polymorphonuclear neutrophils (PMNs) show minimal response to influenza vaccines, they act as critical regulators in co-cultures by enhancing monocyte dynamics, T cell differentiation, and B cell antibody production while simultaneously dampening vaccine-induced cytokine secretion, thereby balancing pro-inflammatory and adaptive immune responses through intercellular crosstalk.
By analyzing nearly 5,000 pan-cancer single-cell RNA sequencing samples, this study reveals that tumor immunity is fundamentally governed by a dichotomy between exhausted CD8+ T cells and CD56dimCD16hi NK cells, where tumors dominated by the latter exhibit high cytolytic activity yet remain refractory to current immune checkpoint blockade therapies.
By integrating spatially resolved proteomics with single-nuclear multiomics, this study reveals that the APOE4/4 genotype drives human microglia in Alzheimer's disease toward dysfunctional terminal states characterized by lost homeostasis, metabolic disruption, and ineffective inflammatory responses, thereby linking genetic risk to specific spatial and molecular immune dysregulation.
In a longitudinal cohort of ART-naive women living with HIV, the study reveals that broadly neutralizing antibody responses are enabled by a viral load-driven trajectory of early systemic immune activation followed by exhaustion, which creates a permissive environment for sustained germinal center activity and antibody maturation.
This study demonstrates that the hypomethylating agent azacytidine restores T cell function and reduces tumor burden in acute myeloid leukemia by reversing epigenetic-driven exhaustion, thereby providing a mechanistic rationale for combining it with T cell-based immunotherapies.
This study reveals that the competitive expansion of memory phenotype regulatory T cells, driven by MLL1-mediated maintenance of TCR expression, is essential for preserving immune tolerance during aging.
Sustained exposure to {Delta}9-tetrahydrocannabinol (THC) in mice infected with the helminth *Nippostrongylus brasiliensis* does not alter parasite burden but reshapes the immune response by restraining innate and T cell effector functions and shifting lung eosinophil and macrophage transcriptional programs toward an anti-inflammatory, stress-adaptive phenotype that mitigates tissue remodeling.
This study demonstrates that *Trypanosoma brucei* infection directly infiltrates the murine uterus, triggering distinct immune remodeling and neuroendocrine dysfunction that collectively disrupt reproductive physiology through independent inflammatory and hormonal pathways.