Abstract
Psoriasis is a chronic inflammatory disorder mediated by elements of both the innate and the adaptive immune system. The first cells involved in the inflammatory response are keratinocytes. These release antimicrobial peptides, such as cathelicidin LL37, which subsequently form complexes with self DNA, enabling the activation of different dendritic cell populations. It is now considered that lymphocyte subsets that have only recently been implicated in psoriasis, such as CD11+ dendritic cells and TH17 cells, play a key role in the pathogenesis of psoriatic lesions. The interleukin 12/23 pathway enables the differentiation and clonal expansion of TH1 and TH17 cells, 2 types of helper T cells that have an essential role in the formation of psoriatic plaques. This pathway not only acts as a bridge between the innate and adaptive immune system, but is also an important therapeutic target, as has been demonstrated clinically with ustekinumab.
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