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Curr Diab Rep. 2019 Jul 31;19(9):69. doi: 10.1007/s11892-019-1193-7.

Extracellular Vesicles in Type 1 Diabetes: Messengers and Regulators.

Author information

1
Human Islet Transplant Laboratory, Department of Surgery, D5.5736, Royal Victoria Hospital, McGill University Health Centre, 1001 Boulevard Décarie, Montréal, QC, H4A 3J1, Canada.
2
Canadian Donation and Transplantation Research Program, Edmonton, Alberta, T6G 2E1, Canada.
3
Human Islet Transplant Laboratory, Department of Surgery, D5.5736, Royal Victoria Hospital, McGill University Health Centre, 1001 Boulevard Décarie, Montréal, QC, H4A 3J1, Canada. steven.paraskevas@mcgill.ca.
4
Canadian Donation and Transplantation Research Program, Edmonton, Alberta, T6G 2E1, Canada. steven.paraskevas@mcgill.ca.

Abstract

PURPOSE OF REVIEW:

Theories about the pathogenesis of type 1 diabetes (T1D) refer to the potential of primary islet inflammatory signaling as a trigger for the loss of self-tolerance leading to disease onset. Emerging evidence suggests that extracellular vesicles (EV) may represent the missing link between inflammation and autoimmunity. Here, we review the evidence for a role of EV in the pathogenesis of T1D, as well as discuss their potential value in the clinical sphere, as biomarkers and therapeutic agents.

RECENT FINDINGS:

EV derived from β cells are enriched in diabetogenic autoantigens and miRNAs that are selectively sorted and packaged. These EV play a pivotal role in antigen presentation and cell to cell communication leading to activation of autoimmune responses. Furthermore, recent evidence suggests the potential of EV as novel tools in clinical diagnostics and therapeutic interventions. In-depth analysis of EV cargo using modern multi-parametric technologies may be useful in enhancing our understanding of EV-mediated immune mechanisms and in identifying robust biomarkers and therapeutic strategies for T1D.

KEYWORDS:

Autoimmunity; Biomarkers; Extracellular vesicles; Islets of Langerhans; Type 1 diabetes; β-cell injury

PMID:
31367976
DOI:
10.1007/s11892-019-1193-7

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