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

(2019) CLINICAL IMMUNOLOGY. 206. p.15-22
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Organization
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
Psoriatic arthritis, Skin and joint inflammation, Cytokines, IL-23/IL-23R pathways, Human monoclonal IL-23 antibodies, Therapeutics, EXTRACELLULAR TRAP FORMATION, T-CELL SUBSET, DOUBLE-BLIND, MONOCLONAL-ANTIBODY, EPIDERMAL HYPERPLASIA, TERMINAL DIFFERENTIATION, RHEUMATOID-ARTHRITIS, OSTEOCLAST FORMATION, CYTOKINE RECEPTOR, PLACEBO

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Citation

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MLA
Nguyen, Cuong Thach, et al. “Pathophysiology and Inhibition of IL-23 Signaling in Psoriatic Arthritis : A Molecular Insight.” CLINICAL IMMUNOLOGY, vol. 206, 2019, pp. 15–22.
APA
Nguyen, C. T., Bloch, Y., Skladanowska, K., Savvides, S., & Adamopoulos, I. E. (2019). Pathophysiology and inhibition of IL-23 signaling in psoriatic arthritis : a molecular insight. CLINICAL IMMUNOLOGY, 206, 15–22.
Chicago author-date
Nguyen, Cuong Thach, Yehudi Bloch, Katarzyna Skladanowska, Savvas Savvides, and Iannis E Adamopoulos. 2019. “Pathophysiology and Inhibition of IL-23 Signaling in Psoriatic Arthritis : A Molecular Insight.” CLINICAL IMMUNOLOGY 206: 15–22.
Chicago author-date (all authors)
Nguyen, Cuong Thach, Yehudi Bloch, Katarzyna Skladanowska, Savvas Savvides, and Iannis E Adamopoulos. 2019. “Pathophysiology and Inhibition of IL-23 Signaling in Psoriatic Arthritis : A Molecular Insight.” CLINICAL IMMUNOLOGY 206: 15–22.
Vancouver
1.
Nguyen CT, Bloch Y, Skladanowska K, Savvides S, Adamopoulos IE. Pathophysiology and inhibition of IL-23 signaling in psoriatic arthritis : a molecular insight. CLINICAL IMMUNOLOGY. 2019;206:15–22.
IEEE
[1]
C. T. Nguyen, Y. Bloch, K. Skladanowska, S. Savvides, and I. E. Adamopoulos, “Pathophysiology and inhibition of IL-23 signaling in psoriatic arthritis : a molecular insight,” CLINICAL IMMUNOLOGY, vol. 206, pp. 15–22, 2019.
@article{8617571,
  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.},
  author       = {Nguyen, Cuong Thach and Bloch, Yehudi and Skladanowska, Katarzyna and Savvides, Savvas and Adamopoulos, Iannis E},
  issn         = {1521-6616},
  journal      = {CLINICAL IMMUNOLOGY},
  keywords     = {Psoriatic arthritis,Skin and joint inflammation,Cytokines,IL-23/IL-23R pathways,Human monoclonal IL-23 antibodies,Therapeutics,EXTRACELLULAR TRAP FORMATION,T-CELL SUBSET,DOUBLE-BLIND,MONOCLONAL-ANTIBODY,EPIDERMAL HYPERPLASIA,TERMINAL DIFFERENTIATION,RHEUMATOID-ARTHRITIS,OSTEOCLAST FORMATION,CYTOKINE RECEPTOR,PLACEBO},
  language     = {eng},
  pages        = {15--22},
  title        = {Pathophysiology and inhibition of IL-23 signaling in psoriatic arthritis : a molecular insight},
  url          = {http://dx.doi.org/10.1016/j.clim.2018.09.002},
  volume       = {206},
  year         = {2019},
}

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