From the TPR pathway and the neuroimmune unit to the cutaneous HPA axis: a neuro-endo-immune cross-talk in rosacea.

The pathogenesis of rosacea is complex, and most of the pathogenesis is not completely clear, but the nervous system, the internal system and the immune system dysregulation is an important factor mediating the pathogenesis of rosacea, yet the three are not a single system's role, it is the mutual influence, the interaction together mediate the pathogenesis of rosacea. The skin is essentially a whole of neural, internal and immune functions. From the neurological aspect, the skin realizes information transmission by means of neural pathways and receptors, and releases neurotrophins and neuropeptides to influence the organism; from the internal level, the skin not only receives multiple signals, but also has an active part, and possesses a local regulatory function similar to that of the hypothalamus-pituitary-adrenal axis; with regard to the immune function, the skin not only relies on physical barriers, but also on immune cells and related molecules to play a defense function, and also participates in the inflammatory response. In terms of immunity, the skin not only relies on the physical barrier, but also on immune cells and related molecules for defense, and also participates in inflammatory reactions. As a multifunctional organ, the skin maintains homeostasis by regulating peripheral neurologic-endoimmune activities, and at the same time receives bi-directional regulation from the central nervous system, the integumentary system and the immune system. This article describes the three systems that work together in the pathogenesis of rosacea, detailing them in three perspectives: the TPR pathway, the neuroimmune cellular unit, and the cutaneous HPA axis. This article provides a certain summary of the pathogenesis of rosacea, as well as reflections on the underlying mechanisms.