Diabetes and associated disorders

This study shows that IFN-α increases HLA-B-restricted antigen presentation in pancreatic β-cells, potentially influencing T1D pathogenesis.

This study estimates that ~6% of insulin-treated diabetic individuals with ambiguous features in British Pakistanis and Bangladeshis have T1D, highlighting the need for autoantibody and C-peptide testing.

The paper uses proteogenomic data to identify circulating proteins associated with type 1 diabetes risk and explores their tissue-specific expression.

The paper investigates how inhibitory KIRs modify HLA class II protective associations in Type 1 Diabetes, finding that iKIRs reduce HLA class II-mediated protection.

This study identifies sex-specific cytokine, chemokine, and growth factor differences in T1D patients and progressors, highlighting potential implications for personalized treatment.

This study shows omega-3 fatty acids reduce CXCL9 expression in MIN6 cells via ARH3, potentially protecting beta cells from immune attack and preventing T1D.

This study shows that blocking CD226 reduces diabetes in NOD mice by enhancing Treg function and reducing effector T cell activity.

This study identifies genetic risk factors for type 1 diabetes in individuals without high-risk HLA-DR3/DR4 haplotypes and develops a new risk score for better classification.

This study shows that activating LRH-1/NR5A2 reduces inflammation in T1D by altering immune cell metabolism and improves human islet function in mice.

This study shows that inhibiting 12-LOX with VLX-1005 delays autoimmune diabetes onset in human gene replacement mice by altering inflammatory pathways and immune cell infiltration.

This study shows that beta cell extracellular vesicle PD-L1 increases in type 1 diabetes and inhibits CD8+ T cell activity, correlating with residual beta cell function.

This study identifies 13 new proinsulin-derived HIPs recognized by human islet-infiltrating CD4+ T cells in T1D, highlighting proinsulin C-peptide's central role in HIP formation.

This study investigates how parasitic infection affects Type 1 diabetes in NOD mice, focusing on the role of osteopontin in immune responses.

This study shows that BET inhibitor I-BET protects β-cells from cytokine-induced death and dysfunction by inhibiting NF-κB signaling and preserving key β-cell genes.

The paper uses network analysis to show that in early insulitis, immune cells preferentially interact with β-cells in specific regions of pancreatic islets in NOD mice.

This study shows that inhibiting PERK reduces autoimmune diabetes risk in mice by decreasing β cell immunogenicity and improving islet function.

This study shows that beta cells lacking Renalase reduce autoimmunity by altering Natural Killer cell activity and enhancing anti-inflammatory responses.

This study shows the IFIH1-A946T risk variant increases T1D risk in females but not males by enhancing IFN I signaling and altering immune cell profiles in NOD mice.

This study shows that m6A methylation, regulated by METTL3, controls the innate immune response in β-cells during T1D onset by modulating OAS mRNA stability.

This review identifies 22 genes associated with early-onset diabetes in Africa, highlighting 9 with pathogenic variants and emphasizing the need for more genetic research in sub-Saharan Africa.

The paper identifies shifts in isoform usage in Tregs associated with Type 1 Diabetes by comparing gene expression between cases and controls.

The paper introduces the T1D Knowledge Portal, a resource for querying genetic and functional data related to type 1 diabetes to aid in hypothesis generation and target discovery.

This study identifies the lncRNA ARGI as a mediator of virus-induced inflammation in pancreatic beta cells linked to type 1 diabetes through allele-specific transcriptional activation.

This study investigates the genotype-phenotype relationship in Wolfram syndrome, finding that specific WFS1 gene variants correlate with earlier onset and more severe disease manifestations.

The paper identifies T1D risk genes and regulatory elements that influence beta cell survival under proinflammatory cytokine exposure using functional genomics and genetics.

This study shows that TYK2 is critical for β-cell development by regulating KRAS and IFN responses, suggesting TYK2 inhibition as a therapeutic target for type 1 diabetes.

The paper describes the integration of a genetic risk prediction platform into the NHS newborn screening program for Type 1 Diabetes, demonstrating a model for population-based genetic research.

The paper identifies a genetic variant that affects transcription factor binding and reduces type 1 diabetes risk in infants by altering thymic gene expression.

This paper uses Mendelian randomization to find that low birth weight and high adult BMI are causally linked to latent autoimmune diabetes in adults, with BMI having a stronger effect than birth weight.

The paper identifies sequence and motif similarities between bacterial and human GAD65, suggesting a potential link between gut microbiome dysbiosis and T1D via immune cross-reactivity.