Diabetes and associated disorders

Nanotherapy-mediated biased antigen-presenting cell reprogramming supports T cell anergy to prevent type 1 diabetes

This paper develops a nanotherapy to reprogram antigen-presenting cells and induce T cell anergy, delaying type 1 diabetes onset in mice.

Insulin-binding B cells can arise in early-stage type 1 diabetes individuals in the absence of somatic hypermutation or insulin autoantibody seropositivity

The paper identifies anti-insulin B cells in early-stage T1D patients without autoantibodies or somatic hypermutation, showing their role in autoimmunity.

A surviving beta cell subpopulation enriched in patients with T1D

Regulon-based clustering of islet scRNA-seq finds an IRF1-high, cytokine-driven beta cell state with reduced identity and autoantigen genes, enriched in type 1 diabetes donors.

Transcriptionally distinct atypical B cell populations contribute to insulin autoreactivity and show differential activation, isotype switching, and somatic hypermutation in early-stage type 1 diabetes individuals

B cells from 24 early-stage type 1 diabetes individuals include four atypical clusters differing in switching and mutation; Cluster 10 had the highest insulin-binding antibody rate (5/16).

Genetic risk and inflammatory signaling converge on cell type-specific regulatory programs in type 1 diabetes

This study identifies T1D-associated SNPs that alter chromatin accessibility at TF binding sites in pancreatic islets, linking genetic risk to cell type-specific regulatory programs.

MicroRNA-146a Deficiency Protects NOD Mice from Autoimmune Diabetes by Enhancing c-Rel-Dependent Regulatory T Cell Function

This study shows that miR146a deficiency protects NOD mice from T1D by enhancing c-Rel-dependent Treg cell function through increased FOXP3 expression.

A Novel PD-L1 Splice Isoform Modulates β Cell Communication in Response to Interferon Signaling

The paper identifies an IFN-induced PD-L1 splice variant, PD-L1Δ3, which is retained intracellularly and fails to suppress T cell activation, altering β cell immune communication in type 1 diabetes.

Cell-based epitope screen identifies a novel B chain-derived Hybrid Insulin Peptide recognized by human and mouse autoreactive CD4 T cells

Harmine Plus Exendin-4 Enhances Remission of Recent-Onset Type 1 Diabetes Following Anti-CD3 Therapy

This study shows that harmine plus exendin-4, when combined with anti-CD3 therapy, promotes beta-cell recovery and reduces immunogenicity, leading to remission of recent-onset type 1 diabetes.

Mitochondrial and protein homeostasis pathways are transcriptionally impaired in islets during type 1 diabetes pathogenesis

This study identifies transcriptional impairments in mitochondrial and protein homeostasis pathways in islets during type 1 diabetes pathogenesis, independent of T-cell infiltration.

SAP loss limits anti-insulin atypical B cell activation and pro-inflammatory CD8 T cells despite preserved Tfh responses to protect against type 1 diabetes

MDA5 and the integrated stress response control sex-specific type 1 diabetes onset in NOD mice

This study shows that MDA5 and the integrated stress response influence sex-specific type 1 diabetes onset in NOD mice, with MDA5 haploinsufficiency protecting males but not females.

Neuropeptide Y4 receptor activation delays autoimmune diabetes by reprogramming β-cell stress and immune tolerance

This study shows that activating the Y4R receptor protects β-cells and modulates islet immunity, delaying autoimmune diabetes in multiple models.

CD38 defines a therapeutically targetable pathogenic T cell population for precision immunotherapy in autoimmune diabetes

The paper identifies CD38 as a marker for pathogenic T cells in T1D and shows that anti-CD38 mAb selectively depletes these cells to prevent diabetes without affecting Tregs.

Consensus Recommendations for the Clinical Management of Wolfram syndrome Using a Delphi Method

This paper develops international clinical guidelines for Wolfram syndrome using a Delphi method, resulting in 35 consensus statements with ≥80% agreement across multiple domains.

Population-Scale, Genotype-First Characterization of Monogenic Diabetes in 374,973 Multi-Ancestry Individuals from the All of Us Research Program

The paper identifies MODY gene variants in a large multi-ancestry cohort, showing incomplete penetrance and comparable diabetes risk between carriers of lower-penetrance variants and high polygenic risk non-carriers.

Coxsackievirus B Escapes Antiviral CD8⁺ T Cells but Triggers Robust CD4⁺ Memory Responses

This study shows that Coxsackievirus B3 evades CD8+ T-cell immunity by downregulating HLA Class I and viral peptide presentation, while inducing robust CD4+ T-cell responses and memory formation.

Beta cell reactivity defines disease-relevant pancreatic CD8 T cells in type 1 diabetes

This study identifies beta cell reactivity as a key feature distinguishing T1D-associated CD8 T cells from other pancreatic T cells.

BCL6 in T cells promotes type 1 diabetes by redirecting fates of insulin-autoreactive B lymphocytes

This paper shows that BCL6 in T cells promotes type 1 diabetes by enabling anti-insulin B cells to become pathogenic, and that blocking BCL6 in T cells prevents diabetes even when insulin-reactive B cells are present.

Carbamylome analysis reveals regulatory roles for lysine carbamylation in β-cell glycolytic and insulin-processing enzymes

The paper identifies carbamylation as a regulatory modification in β-cell metabolism and insulin processing in T1D by analyzing proteomic changes in NOD and MIN6 cells.

Tracking GAD-specific T-cell expansions in Type 1 diabetes by intradermal GAD-Alum challenge

This paper uses intradermal GAD-Alum challenge and scRNA-seq to identify and profile GAD-reactive T cells in type 1 diabetes.

Differences in immune cell profiles around the time of islet autoimmunity seroconversion in children with and without type 1 diabetes

The paper examines immune cell profiles around islet autoimmunity seroconversion in children with and without type 1 diabetes, finding differences in immune cell ratios that may reflect immune maturation disruptions.

Multitissue Multiomics Integration Reveals Tissue-Specific Pathways, Gene Networks, and Drug Candidates for Type 1 Diabetes

From bats to humans: uncovering ISG15 as a new resistance factor in type 1 diabetes

The paper identifies ISG15 as a key factor in viral resistance in pancreatic alpha cells, showing its protective role against coxsackievirus B1 in human islet cells.

Gain-of-function mutation in SKAP2 leads to type 1 diabetes and broader autoimmunity through hyperactive integrin signaling in myeloid cells

Soluble LAG-3 Identifies a Dynamic Early T Cell Activation Window in self-reactivity, Type 1 Diabetes, and Broader Immune Responses.

This study identifies soluble LAG-3 (sLAG-3) as an early biomarker of T cell activation in type 1 diabetes, detectable before islet autoantibody development and associated with beta-cell stress and high-risk HLA genotypes.

Spatial transcriptomics from pancreas and local draining lymph node tissue reveals a lymphotoxin-β signature in human type 1 diabetes

This study uses spatial transcriptomics to identify inflammation signatures in pancreas and lymph node tissues of T1D patients, highlighting LTB and other genes involved in disease pathogenesis.

Shared genetic and neuroimmune architecture links type 1 diabetes with neurocognitive traits

This paper identifies shared genetic and neuroimmune mechanisms linking type 1 diabetes with neurocognitive traits through genome-wide association and single-cell epigenomic analyses.

Role of small intronic RNAs in the crosstalk between immune cells and beta-cells during type 1 diabetes development

The paper identifies two small intronic RNAs, sinR-D and sinR-T, that are transferred between immune cells and beta-cells in type 1 diabetes, with sinR-D promoting beta-cell apoptosis.

Synthetic Immunological Niche Reveals Early Immune Dysregulationand Stratifies Therapeutic Response in Type 1 Diabetes

The paper develops a synthetic immunological niche to identify early immune dysregulation and stratify therapeutic response in Type 1 Diabetes.