Vitiligo is an autoimmune disease clinically characterized by localized or generalized depigmentation of the skin and mucous membranes. The prevalence of this disease in the general population is approximately 0.5%, with no significant gender or racial differences in incidence. Vitiligo results from functional loss of the tyrosinase system within melanocytes in the skin and hair follicles. Its proposed pathogenesis includes autoimmunity, neurohumoral factors, autocytotoxicity, and the melanocyte destruction hypothesis. Among these, the autoimmune theory is currently a major research focus. Animal models of vitiligo can be classified into spontaneous models, chemical-induced depigmentation models, and genetically modified models.

C57BL/6J mice (male and female, 8 weeks old)

Modeling method: Monobenzone cream was applied to the depilated dorsal region. A vitiligo model was established after 50 days.

Evaluation indicators: gross observation, skin depigmentation area score, serum ELISA assay, and HE staining

Gross observation

Skin depigmentation area score and serum ELISA assay

HE staining of skin tissue