Transcriptional regulation on effector T cells in the pathogenesis of psoriasis

Psoriasis is one of the most common inflammatory diseases, characterized by scaly erythematous plaques on the skin. The accumulated evidence on immunopathology of psoriasis suggests that inflammatory reaction is primarily mediated by T helper (Th) cells. The differentiation of Th cells plays important roles in psoriatic progression and it is regulated by transcription factors such as T-bet, GATA3, ROR gamma t, and FOXP3, which can convert naive CD4(+) T cells, respectively, into Th1, Th2, Th17 and Treg subsets. Through the activation of the JAK/STAT and Notch signaling pathways, together with their downstream effector molecules including TNF-alpha, IFN-gamma, IL-17, TGF-beta, these subsets of Th cells are then deeply involved in the pathogenesis of psoriasis. As a result, keratinocytes are abnormally proliferated and abundant inflammatory immune cells are infiltrated in psoriatic lesions. We hypothesize that modulation of the expression of transcription factors for each Th subset could be a new therapeutic target for psoriasis. In this review, we will focus on the recent literature concerning the transcriptional regulation of Th cells in psoriasis.

Automated summary

Psoriasis is an inflammatory disease characterized by scaly erythematous plaques on the skin. The immunopathology of psoriasis suggests that T helper cells are primarily responsible for the inflammatory reaction. These Th cells differentiate into subsets such as Th1, Th2, Th17, and Treg, which play important roles in the pathogenesis of psoriasis. Modulating the expression of transcription factors for each Th subset could be a potential therapeutic target for psoriasis. This review focuses on the transcriptional regulation of Th cells in psoriasis.