Immune-modulatory effects of lenalidomide inhibited the progression of lesions in a vitiligo mouse model

Vitiligo, an autoimmune disorder, is associated with altered cytokine levels and T lymphocytes. Lenalidomide modulates immune system components by altering cytokine production and regulating T-cell stimulation. In this study, effect of lenalidomide was checked on the development of vitiligo lesions, level of various cytokines, and T lymphocytes in the mouse model. The vitiligo mouse model was developed by immunizing C57BL/6 mouse with anti-mouse tyrosine-related protein 2. Lenalidomide was orally given to mice daily, and the effect was observed on the development of vitiligo lesions. The level of T lymphocytes in blood was checked by flow cytometry. Serum cytokine levels were checked by enzyme-linked immunosorbent assay. Vitiligo lesions were found significantly smaller in lenalidomide-treated mice models. It significantly decreased the serum levels of IFN-gamma, TNF-alpha, IL-1 beta, and IL-6 but elevated the levels of IL-4 and IL-10. It non-significantly elevated CD4(+)/CD8(+) T-cell ratio. Lenalidomide had an inhibitory effect on the development of vitiligo lesions in mice models by suppressing the serum level of pro-inflammatory cytokines and increasing anti-inflammatory cytokine levels. It modulated the immune response in vitiligo mice models toward an anti-inflammatory profile suggesting its use in the management of vitiligo.

Automated summary

The study investigated the effects of lenalidomide on vitiligo mouse models, showing that lenalidomide could suppress the development of vitiligo lesions by reducing levels of pro-inflammatory cytokines and increasing levels of anti-inflammatory cytokines, modulating the immune response towards an anti-inflammatory profile.