Role of Regulatory T cells and TGF-β in an Experimental Model of Psoriasis in mice (71.8)

Abstract

Abstract Psoriasis is inflammatory disease with active interactions between the immune system and the skin, which affects approximately 2% of the world’s population and attacks about 10 million people in North America. The pathogenesis of this disease is not completely understood. Regulatory T cells (Tregs) are typically considered to be inhibitors of autoimmune responses, but the role of Tregs in pathogenesis of psoriasis remains largely unclear. Previous works have suggested that overexpression of transforming growth factor beta (TGF-β) is involved in severe skin inflammation similar to psoriasis, but the molecular mechanism by which TGF-β functions in this autoimmune disease remains to be determined. By utilizing an experimentally induced model of psoriasis using Imiquimod (TLR7/8 ligand and potent immune activator), we observed that topical aplication of Imiquimod can induce psoriasis through the IL-23/IL-17 axis in mice. We also found that TGF-β signaling and frequency of Tregs are decreased in this model of psoriasis. To further understand the molecular mechanism of TGF-β in psoriasis we have created transgenic mouse model K14.TGF-β1glo that overexpress TGF-β in epidermal keratinocytes. We are actively investigating the interplay between TGF-β and Treg cells in skin in the pathogenesis of psoriasis.