Interleukin-23 in the Pathogenesis and Treatment of Psoriasis

Ramya Kollipara, MD; Christopher Downing, MD; Rachel Gordon, MD; Stephen Tyring, MD, PhD

Disclosures

Skin Therapy Letter. 2015;20(2) 

In This Article

Abstract and Introduction

Abstract

In the past three decades, major advances have been made in understanding the pathogenesis of psoriasis. The currently accepted theory is that T-cell mediated immune dysregulation triggers keratinocyte hyperproliferation in psoriasis. Recent research indicates that the Th17/interleukin (IL)-23 pathway plays a prominent role in the amplification phase of psoriasis. The discovery of the Th17/IL-23 pathway provides targets for new drug development. This review focuses on the role of IL-23 in psoriasis pathogenesis and the current therapies targeting IL-23 that are in clinical trials.

Introduction

In the past three decades, major strides have been made in understanding the pathogenesis of psoriasis. While psoriasis pathogenesis originally focused on keratinocyte hyperproliferation, the currently accepted theory is that of T-cell mediated immune dysregulation.[1,2] While the T helper cell (Th) 1/interferon-gamma (IFN-γ) pathway was originally heavily implicated in the amplification phase, recent research indicates that the Th17/interleukin (IL)-23 pathway plays the more dominant role.[3] This review focuses on the role of IL-23 in psoriasis pathogenesis and the current therapies targeting IL-23 that are in clinical trials.

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