Potential effects of shift work on skin autoimmune diseases

Front Immunol. 2023 Feb 14:13:1000951. doi: 10.3389/fimmu.2022.1000951. eCollection 2022.

Abstract

Shift work is associated with systemic chronic inflammation, impaired host and tumor defense and dysregulated immune responses to harmless antigens such as allergens or auto-antigens. Thus, shift workers are at higher risk to develop a systemic autoimmune disease and circadian disruption with sleep impairment seem to be the key underlying mechanisms. Presumably, disturbances of the sleep-wake cycle also drive skin-specific autoimmune diseases, but epidemiological and experimental evidence so far is scarce. This review summarizes the effects of shift work, circadian misalignment, poor sleep, and the effect of potential hormonal mediators such as stress mediators or melatonin on skin barrier functions and on innate and adaptive skin immunity. Human studies as well as animal models were considered. We will also address advantages and potential pitfalls in animal models of shift work, and possible confounders that could drive skin autoimmune diseases in shift workers such as adverse lifestyle habits and psychosocial influences. Finally, we will outline feasible countermeasures that may reduce the risk of systemic and skin autoimmunity in shift workers, as well as treatment options and highlight outstanding questions that should be addressed in future studies.

Keywords: autoimmune; circadian; cortisol; inflammation; melatonin; shift work; skin; sleep.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Autoimmune Diseases* / etiology
  • Autoimmune Diseases* / immunology
  • Autoimmunity
  • Chronic Disease
  • Humans
  • Inflammation / etiology
  • Inflammation / immunology
  • Shift Work Schedule* / adverse effects
  • Skin / immunology
  • Skin Diseases* / etiology
  • Skin Diseases* / immunology
  • Sleep Disorders, Circadian Rhythm* / etiology
  • Sleep Disorders, Circadian Rhythm* / immunology

Grants and funding

This study was supported by grants dedicated to Jennifer Hundt and Tanja Lange of the Research Training Group “Defining and Targeting Autoimmune Pre-Disease” (GRK 2633/1 – 2021, 429175970) and the Excellence Cluster “Precision Medicine in Chronic Inflammation” (EXC 2167), both from the Deutsche Forschungsgemeinschaft.