Psoriasis is a chronic inflammatory cutaneous disease with a complex pathogenesis that remains incompletely understood. New data suggest that psoriasis severity may be more accurately assessed by examining inflammation, oxidative stress, and hormones, although further research is needed to substantiate the clinical value of these biomarkers. The multifactorial causes of psoriasis encompass metabolic deregulations, such as lipid alterations that favor inflammation, exacerbate immune cell activity, and worsen the disease symptomatology. The pathophysiological link between psoriasis and obesity may be revealed through a crosstalk between adipocytes and the immune system, mediated by diverse soluble mediators, including adipokines. In this autoimmune disease, dermal mesenchymal stem cells (MSCs) are potential cellular players that connect autoimmune mechanisms, inflammation, and dysregulation of lipid metabolism. Networks of soluble factors, immune and non-immune cells, and MSCs mediate the inflammatory state in psoriasis. In many recent studies, the relapse has been associated with the potential role of MSCs in this process, endorsing MSCs as a new therapeutic reservoir in psoriasis. Thus, in our review, we aimed to evaluate the potential connection between autoimmunity, inflammation, and dermal mesenchymal stem cells, along with dysregulation of lipid metabolism, to elucidate the identity of psoriasis and identify potential new diagnostic and/or therapeutic targets.