Islet–immune cell communication in diabetes: mechanisms, extracellular vesicles, and therapeutic opportunities

Type 1 (autoimmune) and Type 2 (metabolic) diabetes both arise from progressive failure of pancreatic islet cells, but the immune system plays a central and increasingly recognized role in both. In autoimmune diabetes, immune cells directly attack and destroy insulin-producing β-cells, while in metabolic diabetes, chronic low-grade inflammation and immune cell infiltration accompany and accelerate islet dysfunction under metabolic stress. Rather than being a passive target, the islet actively participates in this process: stressed islet cells release signals, including protein, lipid, and nucleic acid cargo packaged in extracellular vesicles, that recruit and shape the behavior of immune populations. These immune cells, in turn, feed signals back to the islet. This bidirectional dialogue is emerging as a shared thread linking otherwise distinct forms of diabetes.This Research Topic aims to bring together current work on how stressed islet cells communicate with infiltrating and resident immune cells, and how immune populations feed signals back to islet cells in return. A particular focus is the specific contribution of extracellular vesicles and other non-canonical modes of intercellular communication to this exchange. A central open question is which of these communication pathways distinguish autoimmune from metabolic diabetes, and which are shared between the two, since resolving this could clarify disease mechanisms that have so far been studied largely in isolation. Recent advances in spatial, temporal, and single-cell approaches now make it possible to dissect this dialogue with a precision that was previously unavailable, revealing cell-type-specific signals and their timing within disease progression. Building on these advances, this Topic also aims to evaluate whether components of islet–immune communication can be exploited as biomarkers of disease onset and progression, or as targets for therapeutic intervention, moving this area of research from mechanistic insight toward clinical application.We invite contributions addressing the following themes, spanning molecular, cellular, and translational perspectives on islet–immune crosstalk in diabetes:• Molecular dialogue between islet and immune cells• Extracellular vesicles and non-canonical intercellular communication• β-cell stress, inflammation, and immune activation• Immune-mediated islet dysfunction and destruction• Islet–immune communication in autoimmune diabetes• Islet–immune communication in metabolic diabetes• Spatial, temporal, and single-cell approaches to islet–immune dialogue• Biomarker and therapeutic opportunities arising from islet–immune signaling• Novel methodologies and technical insights to study Islet–immune communicationWe welcome Original Research, Reviews, Mini Reviews, and Perspective articles that advance mechanistic understanding of islet–immune communication or its translation into diagnostic and therapeutic strategies, including studies using in vitro, animal, and human samples. Topic editors: Romano Regazzi, Guido Sebastiani Source: https://www.frontiersin.org/research-topics/85472/islet-immune-cell-communication-in-diabetes-mechanisms-extracellular-vesicles-and-therapeutic-opportunities