title: Relationship between redox status and cell fate in immunity and autoimmunity.
abstract: CONCLUSIONS
  The signaling function of redox molecules is essential for an efficient and proper execution of a large number of cellular processes, contributing to the maintenance of cell homeostasis. Excessive oxidative stress is considered as playing an important role in the pathogenesis of autoimmune diseases by enhancing inflammation and breaking down the immunological tolerance through protein structural modifications that induce the appearance of neo/cryptic epitopes.
  
  
  BACKGROUND
  There is a complex reciprocal relationship between oxidative stress and both apoptosis and autophagy, which is essential to determine cell fate. This is especially relevant in the context of autoimmune disorders in which apoptosis and autophagy play a crucial pathogenic role.
  
  
  RESULTS
  In this review, we describe the latest developments with regard to the involvement of redox molecules in the initiation and progression of autoimmune disorders, focusing on their role in cell fate regulation. We also discuss new therapeutic approaches that target oxidative stress in the treatment of these disorders. The administration of antioxidants is scarcely studied in autoimmunity, and future analyses are needed to assess its beneficial effects in preventing or ameliorating these diseases.
  
  
  CONCLUSIONS
  Deciphering the intricate relationships between oxidative stress and both apoptosis and autophagy in the context of autoimmunity could be critical in elucidating key pathogenic mechanisms and could lead to novel interventions for the clinical management of autoimmune diseases.
authors.affiliation: 1 Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità , Rome, Italy .
authors.forename: Elena
authors.initials: E
authors.lastname: Ortona
authors.forename: Angela
authors.initials: A
authors.lastname: Maselli
authors.forename: Federica
authors.initials: F
authors.lastname: Delunardo
authors.forename: Tania
authors.initials: T
authors.lastname: Colasanti
authors.forename: Antonello
authors.initials: A
authors.lastname: Giovannetti
authors.forename: Marina
authors.initials: M
authors.lastname: Pierdominici
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics / Q000502:physiology; D015551:Autoimmunity / Q000502:physiology*; D001343:Autophagy / Q000276:immunology* / Q000502:physiology; D006801:Humans; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species