Psoriasis treated by UVB in two ways: more Vitamin D, less cholesterol
On the role of cholesterol, vitamin D, lumisterol, and tachysterol signaling in psoriasis
Journal of Investigative Dermatology (2026) doi:10.1016/j.jid.2026.01.005
Andrzej T. Slominski1,2,3 aslominski@uabmc.edu ∙ Robert C. Tuckey4 ∙ Radomir M. Slominski5 ∙ Michael F. Holick 6 ∙ Anton M. Jetten7
Recent advances in skin omics indicate that increased cholesterol synthesis and downstream cholesterol signaling can play a role in the etiology, progression, and presentation of psoriasis through the upregulation of IL-17 signaling and expression of proinflammatory cytokines (Møller et al, 2025; Randon and Ward, 2025). Cholesterol and its downstream oxysterols generated through the action of cytochrome P450 (CYP) enzymes or structural modification by free radicals act as ligands for several nuclear receptors, including retinoic acid orphan receptor (ROR)γ, which have been reported to regulate proinflammatory signaling pathways (Figure 1a) (Jetten and Cook, 2020). Cholesterol and oxysterols through these receptors can contribute to the proinflammatory environment. Therefore, these receptors may represent therapeutic targets for the treatment of psoriasis and other inflammatory disorders.
Clinical Implications
- UVB attenuates cholesterol production and stimulates the generation of vitamin D, lumisterol, tachysterol, and cutaneous expression of CYP11A1.
- Cholesterol and oxysterols are proinflammatory in part through the activation of retinoic acid orphan receptor (ROR)γ.
- Vitamin D, lumisterol, and tachysterol hydroxyderivatives exert anti-inflammatory activities through the activation of the vitamin D receptor and inverse agonism on RORγ.
- Stimulation of local vitamin D, lumisterol, and tachysterol signaling represents a realistic strategy for the therapy of psoriasis.
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