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The role of IL ‐23 and the IL ‐23/ T H 17 immune axis in the pathogenesis and treatment of psoriasis
Author(s) -
Girolomoni G.,
Strohal R.,
Puig L.,
Bachelez H.,
Barker J.,
Boehncke W.H.,
Prinz J.C.
Publication year - 2017
Publication title -
journal of the european academy of dermatology and venereology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.655
H-Index - 107
eISSN - 1468-3083
pISSN - 0926-9959
DOI - 10.1111/jdv.14433
Subject(s) - psoriasis , medicine , immune system , interleukin 23 , pathogenesis , immunology , cytokine , population , disease , interleukin 17 , environmental health
Psoriasis is a chronic, immune‐mediated disease affecting more than 100 million people worldwide and up to 2.2% of the UK population. The aetiology of psoriasis is thought to originate from an interplay of genetic, environmental, infectious and lifestyle factors. The manner in which genetic and environmental factors interact to contribute to the molecular disease mechanisms has remained elusive. However, the interleukin 23 ( IL ‐23)/T‐helper 17 ( T H 17) immune axis has been identified as a major immune pathway in psoriasis disease pathogenesis. Central to this pathway is the cytokine IL ‐23, a heterodimer composed of a p40 subunit also found in IL ‐12 and a p19 subunit exclusive to IL ‐23. IL ‐23 is important for maintaining T H 17 responses, and levels of IL ‐23 are elevated in psoriatic skin compared with non‐lesional skin. A number of agents that specifically inhibit IL ‐23p19 are currently in development for the treatment of moderate‐to‐severe plaque psoriasis, with recent clinical trials demonstrating efficacy with a good safety and tolerability profile. These data support the role of this cytokine in the pathogenesis of psoriasis. A better understanding of the IL ‐23/ T H 17 immune axis is vital and will promote the development of additional targets for psoriasis and other inflammatory diseases that share similar genetic aetiology and pathogenetic pathways.