**1. Introduction**

Environment-driven metabolic adaptations perform important roles in regulating the immune system. Specific metabolic pathways control T-cell activation/proliferation/differentiation and regulate the switch towards either pro- or anti-inflammatory responses: it, therefore, seems rational that metabolic trepidations can alter selfimmune tolerance [1]. Aberrant metabolic pathways constitute a molecular snapshot of the cellular processes that are exaggerated during disease pathogenesis [2]. This

immune-metabolic interactome can orchestrate the choreography of interleukin (IL)-17-producing T helper (Th17) cells-induced pathogenicity in psoriatic patients, manifested as a 'psoriatic march', ultimately resulting in the development of a variety of psoriasis-associated co-morbidities [3]. Metabolic anomalies influencing the T regulatory cells (Treg)/Th17 axis play a paramount role in the pathophysiology of psoriasis, so it is imperative to understand the close linkage between metabolic pathways and immune cell function: this may unveil specific interventional targets and suggest indirect dietary styles and repositioning of metabolic drugs that beneficially impact the abnormal T-cell metabolism [4].
