In mouse studies, topical calcipotriol administration to the ear and dorsal skin led to a dose-dependent increase in the production of the epithelial cell-derived cytokine TSLP by keratinocytes , and triggered atopic dermatitis at high concentrations.  This upregulation of TSLP production due to calcipotriol application is thought to be mediated through the coactivation of vitamin D receptor / RXRα and vitamin D receptor/ RXRβ heterodimers. As psoriasis is typically thought to be partially driven by Th1 / Th17 inflammatory cytokines,  calcipotriol treatment at appropriate concentrations may alleviate psoriasis symptoms by repressing Th1/Th17 inflammation through TSLP production, which is linked to a Th2 response. However, it is important to note that this has not yet been confirmed.
The most frequent adverse reactions include burning, stinging, rash, red, bumpy rash, redness, itching, moderate tingling or prickling feeling, and allergic rash. Local adverse reactions that have been reported with topical corticosteroids include itching, irritation, dryness, folliculitis (swelling of the hair follicles), hypertrichosis (excessive hair growth), acneiform eruptions (acne or rashes resembling acne), hypopigmentation (loss of skin color), perioral dermatitis (rash around the mouth), allergic contact dermatitis (rash), secondary infections, skin atrophy (thinning), striae (lines on the skin), and miliaria (rash due to blocking of the sweat glands, 'prickly heat').