Year: 2015
Type: article
Abstract: Psoriasis is a chronic inflammatory skin disease that affects approximately 2% of the world's population.Accumulated knowledge regarding the role of IL-6 in psoriasis makes it a good candidate for therapy.However, several reports have now demonstrated the onset and/or worsening of psoriasis after treatment with the humanized anti-IL-6R antibody, tocilizumab.Given this paradoxical onset of psoriasis after tocilizumab treatment we hypothesized that under inflammatory conditions, the blockade of IL-6R causes IL-6 to be liberated into the periphery where it can bind alternative receptors causing off-target effects that, in the presence of TGF-β and IL-23, may cause the differentiation of naïve CD4 cells towards a Th17 phenotype and away from the suppressive regulatory T cell phenotype.Th17 cells can then produce other proinflammatory cytokines such as IL-17 and IL-22, which have been shown to be required for initiating and sustaining epidermal hyperplasia associated with psoriasis.independent pathways in the development of interleukin 17producing T helper cells.
Author: Nilmarie Ayala‐Fontanez
Institution: Case Western Reserve University
Language: English
Subfield: Immunology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W2595064265