Diabetes and associated disorders

The paper shows that common genetic variants influence disease risk and severity in monogenic diabetes, modifying clinical outcomes in individuals with pathogenic variants.

This study demonstrates that non-myeloablative conditioning with anti-CD117 antibodies and HCT can induce durable mixed chimerism and cure autoimmune diabetes in NOD mice.

This study investigates how Coxsackievirus B (CVB) infection affects different cell types in human pancreatic islets using single-cell RNA sequencing, revealing cell-specific transcriptional and functional responses.

This study shows that beta cell dysfunction occurs in type 1 diabetes independently of T cell infiltration, using human pancreas tissue slices from recently diagnosed patients.

This study performs a genome-wide association study of T1D stratified by HLA DR3 and DR4 status, revealing genetic and biological heterogeneity in T1D progression.

This paper develops a pipeline for translating type 1 diabetes polygenic risk scores into clinical use, showing they can distinguish type 1 from type 2 diabetes and identify high-risk individuals.

This study shows that elevated plasma proinsulin and PI:C ratios predict diabetes onset in NOD mice and correlate with reduced beta cell Pc1/3 expression.

This study shows that inhibiting formate production in CD8+ T cells delays type 1 diabetes onset in mice by reducing their activation and effector function.

Laser-microdissected islets of 3 multiple-autoantibody-positive stage 1 type 1 diabetes donors versus matched controls show 202 altered proteins: immune and glycolytic up, translation and ER-stress proteins down.

This study identifies aberrant immune regulation and stem-like CD8+ T cells in pancreatic lymph nodes during type 1 diabetes development using mass cytometry and single-cell RNA sequencing.

The paper analyzes immune cell changes in human pancreas-draining lymphatic tissues before and after T1D onset, identifying proinflammatory patterns and genetic risk correlations.

This paper develops a bioinformatics pipeline to identify key transcription factors regulating type 1 diabetes transcriptomes, revealing novel molecular drivers and therapeutic targets.

The paper assesses the genetic evidence for NEUROD1, PDX1, APPL1, and WFS1 in MODY, finding that only NEUROD1 and PDX1 variants are enriched, while APPL1 and WFS1 are not.

This study shows that TYK2 inhibitors reduce islet inflammation and delay type 1 diabetes onset in mice by modulating immune and endocrine responses.

This study shows that AAT-overexpressing MSCs reverse T1D in NOD mice by enhancing Treg function and inducing CD8+ T cell exhaustion.

This study shows that EVs deplete GGA2 in beta cells, causing Golgi acidification and altering the MHC class I immunopeptidome through premature cathepsin activation.

The paper identifies unique phenotypic and BCR repertoire features of pancreatic islet antigen-reactive B cells in prediabetic and recent-onset type 1 diabetes individuals compared to non-diabetic donors.

The paper redirects TCR specificity in regulatory T cells toward class I HLA antigens to enhance tissue-specific homing in Type 1 Diabetes.

This study identifies SH2B3 as a critical regulator of T cell tolerance in T1D, showing that its deficiency enhances cytokine signaling and promotes islet destruction.

The paper uses imaging mass cytometry to analyze human pancreatic samples and identifies early β-cell dysfunction and immune changes in type 1 diabetes progression.

This study investigates islet cell dysfunction in type 1 diabetes by integrating electrophysiological, transcriptomic, and machine learning analyses of human islet cells from T1D donors.

This study shows that inhibiting NAMPT reduces inflammation and beta-cell damage in T1D by blocking cytokine-mediated immune responses in mice.

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 identifies key genes and monocytes in T1D pathogenesis using scRNA-seq, bulk RNA-seq, and experimental validation, showing high diagnostic model efficiency.

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.