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

Cuong Thach Nguyen, Yehudi Bloch, Katarzyna Składanowska, Savvas N. Savvides, Iannis Adamopoulos

Research output: Contribution to journalArticle

2 Citations (Scopus)

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.

Original languageEnglish (US)
JournalClinical Immunology
DOIs
StateAccepted/In press - Jan 1 2018

Fingerprint

Interleukin-23
Psoriatic Arthritis
Interleukin Receptors
Adaptive Immunity
Transducers
Psoriasis
Innate Immunity
Arthritis
Therapeutics

Keywords

  • Cytokines
  • Human monoclonal IL-23 antibodies
  • IL-23/IL-23R pathways
  • Psoriatic arthritis
  • Skin and joint inflammation
  • Therapeutics

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Pathophysiology and inhibition of IL-23 signaling in psoriatic arthritis : A molecular insight. / Nguyen, Cuong Thach; Bloch, Yehudi; Składanowska, Katarzyna; Savvides, Savvas N.; Adamopoulos, Iannis.

In: Clinical Immunology, 01.01.2018.

Research output: Contribution to journalArticle

Nguyen, Cuong Thach ; Bloch, Yehudi ; Składanowska, Katarzyna ; Savvides, Savvas N. ; Adamopoulos, Iannis. / Pathophysiology and inhibition of IL-23 signaling in psoriatic arthritis : A molecular insight. In: Clinical Immunology. 2018.
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