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Reijonen, H.

Publications and source records attributed to Reijonen, H..

2 recordsLinked to original sources

Loss of Exocytosis Protein DOC2B is an Early Event in Type 1 Diabetes Development

Abstract: Type 1 diabetes (T1D) affects millions worldwide, yet few non-invasive biomarkers detect immune-mediated {beta}-cell dysfunction during the presymptomatic phase, a critical window for therapeutic intervention. Previously, we identified reduced double C2-like domain containing beta protein (DOC2B) levels in circulating platelets as a marker of reduced {beta}-cell function in early-onset T1D cohorts and nonobese diabetic (NOD) mice. Here, we assessed whether plasma DOC2B could serve as a sensitive early biomarker of T1D progression risk in the autoantibody-positive pediatric cohort (progressors vs non-progressors) from the longitudinal Diabetes Evaluation in Washington (DEW-IT) study; T1D patients and non-diabetic cohorts from the DEW-IT study served as controls. At pre-onset, progressors showed a decline in DOC2B that preceded measurable changes in random C-peptide and HbA1c levels, while non-progressors maintained stable levels. These observations were further supported by our analysis in prediabetic NOD mice. Comparisons of plasma levels pre- and post-clinical islet transplantation in long-standing T1D patients highlights its potential utility as a reporter of {beta}-cell functional mass. Together, these findings suggest that DOC2B decline may precede C-peptide decline in early presymptomatic T1D progression. This work could have significant future implications for clinical trial stratification and assessing response outcomes to disease-modifying or cell replacement therapies.

physiology↗

Proinflammatory circulating extracellular vesicles from type 1 diabetes patients contribute to beta cell cytotoxicity and disease pathogenicity

In Type 1 diabetes (T1D), {beta}-cell loss and autoimmunity initiate years before disease diagnosis. However, the mechanisms remain unknown. Here, we investigated the role and mechanisms of circulating extracellular vesicles (cEVs) on T1D pathogenesis and {beta}-cell cytotoxicity. We used cEVs isolated from healthy donors (HD), T1D, multiple autoantibody-positive (AAb+), pre- and post-islet transplantation T1D subjects, NOD-T1D mice, and T1D PBMCs. Patient T1D-cEVs significantly induced apoptosis in vitro in human {beta}-cells but not -cells compared to HD-cEVs. cEVs from AAb+ subjects and pre-diabetic mice were cytotoxic, demonstrating that cEV-induced {beta}-cell cytotoxicity precedes T1D onset and diagnosis. cEV reduction in prediabetic NOD-T1D mice improved {beta}-cell health implying cEV contribution to T1D development. Proteomic analysis of patient T1D-cEVs found several proinflammatory proteins, including interferon gamma, which induced {beta}-cell cytotoxicity. Our data using cEVs from pre- and post-islet transplant and PBMC-EVs from T1D patients implicated immune cells as a potential cellular source of cytotoxic cEVs in T1D. Collectively, our data using T1D patient samples coupled with studies in mice demonstrate that cEVs contribute to {beta}-cell cytotoxicity and to the progression of T1D pathogenicity. Our study is one of the first to demonstrate a functional role of the proinflammatory cEV protein cargo on glucose homeostasis, {beta}-cell health, and insulitis. Our studies on T1D-cEVs may lead to discovery of novel biomarkers and therapeutic targets for T1D.

cell biology↗