Abstract
Introduction:
Psoriasis is a chronic inflammatory skin disorder determined by the activation of several immune cells and resident tissue cells. Various cytokines mediate inflammatory signals, including IL-23, which is an important factor involved in the differentiation of T helper (Th17) cells.
Areas covered:
Increasing evidence suggests that IL-23 is a central cytokine to the pathogenesis of psoriasis. An overview on both experimental and human data will be reported in order to support the hypothesis of a key pathogenic role of IL-23/Th17 axis.
Expert opinion:
Targeting IL-23 might be a more selective, valid and effective therapeutic approach, which, potentially, may show important advantages in terms of long-term efficacy and safety in the treatment of psoriasis.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Animals
-
Antibodies, Monoclonal / therapeutic use*
-
Antigen-Presenting Cells / metabolism
-
Bacterial Infections / immunology
-
Cell Differentiation
-
Clinical Trials as Topic
-
Cytokines / physiology
-
Drug Evaluation, Preclinical
-
Genetic Predisposition to Disease
-
Humans
-
Interleukin-12 Subunit p40 / antagonists & inhibitors
-
Interleukin-12 Subunit p40 / genetics
-
Interleukin-23 / antagonists & inhibitors
-
Interleukin-23 / genetics
-
Interleukin-23 / physiology*
-
Interleukin-23 Subunit p19 / antagonists & inhibitors
-
Interleukin-23 Subunit p19 / genetics
-
Interleukin-23 Subunit p19 / physiology
-
Keratinocytes / metabolism
-
Mice
-
Mice, Knockout
-
Molecular Targeted Therapy*
-
Psoriasis / genetics
-
Psoriasis / immunology
-
Psoriasis / physiopathology*
-
Receptors, Interleukin / antagonists & inhibitors
-
Receptors, Interleukin / physiology
-
Signal Transduction
-
T-Lymphocyte Subsets / immunology
-
Th17 Cells / immunology
Substances
-
Antibodies, Monoclonal
-
Cytokines
-
IL23R protein, human
-
Interleukin-12 Subunit p40
-
Interleukin-23
-
Interleukin-23 Subunit p19
-
Receptors, Interleukin