Novel intercellular communication routes in autoinflammation: beyond classical immune signaling

Effective immune responses depend on tightly regulated communication between immune and non-immune cells. Beyond classical cytokine- and receptor-mediated signaling, recent advances have identified a variety of non-canonical mechanisms that enable both direct, contact-dependent and indirect, extracellular mediator-driven intercellular communication. These emerging pathways play key roles in immune activation, functional reprogramming, and the maintenance, or disruption, of tissue homeostasis. Increasing evidence indicates that their dysregulation contributes to the initiation and progression of autoinflammatory disorders, where innate immune-mediated, sterile tissue inflammation can be amplified and sustained through cell-cell interactions and extracellular communication routes, including extracellular vesicles and extracellular traps. However, across the autoinflammation field, these mechanisms are often studied in isolation, and their convergence into shared amplification circuits remains insufficiently defined.This Research Topic aims to highlight novel modes of intercellular communication involved in innate immune–mediated pathology in autoinflammatory disorders, with emphasis on mechanisms that converge to amplify sterile inflammation (rather than single-mechanism descriptions in broad inflammation). Topics of interest include extracellular vesicles (exosomes, microvesicles, apoptotic bodies) as mediators of immune regulation and antigen transfer, including their cargo of regulatory RNAs such as miRNAs, lncRNAs, and other non-coding RNAs; extracellular traps (NETs and related structures) and their contribution to inflammation, tissue damage, and the exposure and dissemination of immunostimulatory self-derived inflammatory material; tunneling nanotubes and other contact-dependent communication mechanisms; and emerging pathways that control immune cell activation, differentiation, and metabolic and functional reprogramming. We particularly encourage submissions that clarify mechanistic links between at least two of these communication routes in autoinflammatory contexts.We particularly welcome studies addressing the role of these mechanisms in systemic and organ-specific autoinflammatory disorders, including conditions driven by innate immune dysregulation (e.g., inflammasomopathies/IL-1–mediated syndromes and type I interferonopathies). Where relevant, we also welcome contributions at the interface of autoinflammation, and autoimmunity provided the primary focus remains on autoinflammatory pathways and disease relevance. Contributions exploring interactions between immune, stromal, endothelial, or metabolic tissues, as well as the role of immunometabolic communication in sterile inflammatory settings with clear autoinflammatory relevance, are also encouraged. Article types may include original research, reviews, mini-reviews, and perspectives focusing on mechanistic insights, disease relevance, biomarker potential, or therapeutic implications, including, but not limited to:• extracellular vesicles• NETs• Nanotubes• Trogocytosis• metabolic signals• cell-tissue communication• cell-cell communication Topic editors: Natalia Cuesta Rubio, Olga Barreiro Source: https://www.frontiersin.org/research-topics/78965/novel-intercellular-communication-routes-in-autoinflammation-beyond-classical-immune-signaling