Advances in endoplasmic reticulum stress response in immune-associated skin diseases: Mini-review

The skin protects the body from external allergens and pathogens. Disruption of the physiological state of the skin is a hallmark of many immune-associated skin disorders and is well-characterized in disease states such as psoriasis, vitiligo, and systemic lupus erythematosus (SLE). The endoplasmic reticulum (ER) is a crucial organelle within the cell responsible for functions such as protein synthesis, modification and folding. Endoplasmic reticulum stress (ERS) is characterized as an intracellular condition of stress that typically arises from aberrant protein synthesis or environmental changes. Various stimuli such as ischemia, hypoxia, and oxidative stress can trigger ERS, resulting in the misfolding of newly synthesized proteins and the activation of the unfolded protein response (UPR). Emerging evidence indicates that UPR signaling modules have fundamental roles in multiple physiological processes beyond the homeostatic control of protein folding including the pathogenesis of several immune-related skin disorders. We summarize the potential role of ER stress and the UPR in immune-associated skin diseases. This review aims to explore the mechanisms underlying ERS response in these immune-associated skin diseases, offering valuable insights for further research. Understanding the molecular mechanism of UPR activation and ER stress may represent a novel target for drug discovery and innovative therapeutic strategies in the context of immune-associated skin diseases.