Περίληψη:
Autophagy is a major self-degradative process through which cytoplasmic material, including damaged organelles and proteins, are delivered and degraded in the lysosome. Autophagy represents a dynamic recycling system that produces new building blocks and energy, essential for cellular renovation, physiology, and homeostasis. Principal autophagy triggers include starvation, pathogens, and stress. Autophagy plays also a pivotal role in immune response regulation, including immune cell differentiation, antigen presentation and the generation of T effector responses, the development of protective immunity against pathogens, and the coordination of immunometabolic signals. A plethora of studies propose that both impaired and overactive autophagic processes contribute to the pathogenesis of human disorders, including infections, cancer, atherosclerosis, auto-immune and neurodegenerative diseases. Autophagy has been also implicated in the development and progression of allergen-driven airway inflammation and remodeling. Here, we provide an overview of recent studies pertinent to the biology of autophagy and molecular pathways controlling its activation, we discuss autophagy-mediated beneficial and detrimental effects in animal models of allergic diseases and illuminate new advances on the role of autophagy in the pathogen-esis of human asthma. We conclude contemplating the potential of targeting autophagy as a novel therapeutic approach for the management of allergic responses and linked asthmatic disease. © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article.
Λέξεις-κλειδιά:
allergic airway inflammation; allergic asthma; allergic disease; allergic reaction; autophagy (cellular); human; immunopathogenesis; nonhuman; pathogenesis; Review; animal; asthma; autophagy; biological model; complication; genetic transcription; genetics; hypersensitivity; immunology; inflammation; pathology, Animals; Asthma; Autophagy; Humans; Hypersensitivity; Inflammation; Models, Biological; Transcription, Genetic
