Pathophysiology and inhibition of IL-23 signaling in psoriatic arthritis: A molecular insight

Cuong Thach Nguyen; Yehudi Bloch; Katarzyna Składanowska; Savvas N Savvides; Iannis E Adamopoulos

doi:10.1016/j.clim.2018.09.002

Pathophysiology and inhibition of IL-23 signaling in psoriatic arthritis: A molecular insight

Clin Immunol. 2019 Sep:206:15-22. doi: 10.1016/j.clim.2018.09.002. Epub 2018 Sep 6.

Authors

Cuong Thach Nguyen¹, Yehudi Bloch², Katarzyna Składanowska², Savvas N Savvides², Iannis E Adamopoulos³

Affiliations

¹ Department of Internal Medicine, Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, CA, USA.
² Department of Biochemistry and Microbiology, Ghent University, Technologiepark 927, Ghent 9052, Belgium; VIB Center for Inflammation Research, Technologiepark 927, Ghent 9052, Belgium.
³ Department of Internal Medicine, Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, CA, USA; Shriners Hospitals for Children Northern California, Institute for Pediatric Regenerative Medicine, CA, USA. Electronic address: iannis@ucdavis.edu.

Abstract

Psoriatic arthritis (PsA) is a chronic inflammatory arthritis of unknown etiology, and currently the cellular and molecular interactions that dictate its pathogenesis remain elusive. A role of the interleukin-23 (IL-23)/IL-23R (IL-23 receptor) interaction in the development of psoriasis and PsA is well established. As IL-23 regulates the differentiation and activation of innate and adaptive immunity, it pertains to a very complex pathophysiology involving a plethora of effectors and transducers. In this review, we will discuss recent advances on the cellular and molecular pathophysiological mechanisms that regulate the initiation and progression of PsA as well as new therapeutic approaches for IL-23/IL-23R targeted therapeutics.

Keywords: Cytokines; Human monoclonal IL-23 antibodies; IL-23/IL-23R pathways; Psoriatic arthritis; Skin and joint inflammation; Therapeutics.

Publication types

Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review

MeSH terms

Antibodies, Monoclonal, Humanized / pharmacology
Antibodies, Monoclonal, Humanized / therapeutic use
Arthritis, Psoriatic / drug therapy*
Arthritis, Psoriatic / physiopathology*
Dermatologic Agents / pharmacology*
Dermatologic Agents / therapeutic use
Humans
Interleukin-23 / antagonists & inhibitors*
Signal Transduction / drug effects*
Ustekinumab / pharmacology
Ustekinumab / therapeutic use

Substances

Antibodies, Monoclonal, Humanized
Dermatologic Agents
Interleukin-23
secukinumab
Ustekinumab

Grants and funding

R01 AR062173/AR/NIAMS NIH HHS/United States