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Review
. 2016 Sep;20(5):375-431.
doi: 10.1177/1203475416655705. Epub 2016 Jul 15.

2016 Addendum to the Canadian Guidelines for the Management of Plaque Psoriasis 2009

Canadian Psoriasis Guidelines Addendum Committee
Collaborators
Review

2016 Addendum to the Canadian Guidelines for the Management of Plaque Psoriasis 2009

Canadian Psoriasis Guidelines Addendum Committee. J Cutan Med Surg. 2016 Sep.
No abstract available

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Figures

Figure 1.
Figure 1.
Proposed psoriasis immunopathogenesis.
Figure 1.
Figure 1.
Mechanism of action for biologic agents targeting TNF-α and IL-12/23. Biologic therapies that target TNF-α and IL-12/23 are shown. Anticytokine therapies include infliximab, adalimumab, etanercept (anti-TNFs), and a monoclonal antibody against IL-12 and IL-23 (ustekinumab). Anti-TNF strategies have 3 variants: a humanized chimeric anti–TNF-α monoclonal antibody, a fully human monoclonal anti–TNF-α antibody, and a human p75 TNF-receptor Fc fusion protein. Finally, blocking of IL-12 and IL-23 is achieved by means of antibodies targeting the common p40 chain of these cytokines. Essentially, ustekinumab targets differentiation cytokines for Th1 and Th17, blunting inflammation and preventing abnormal keratinocyte differentiation and proliferation. Sources: Data from Garber K. Psoriasis: from bed to bench and back. Nat Biotechnol. 2011;29:563-566; FDA Dermatological and Opthalmic Drugs Advisory Committee meeting, January 17, 2008; and Nestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med. 2009;361(5):496-509.
Figure 1.
Figure 1.
Comorbidities in psoriasis.
Figure 1.
Figure 1.
Targets of new biologics and small molecules in psoriasis. New biologics and small molecules under development for the treatment of plaque psoriasis. Dendritic cells produce IL-12 and IL-23, implicated in Th1 and Th17 lymphocyte differentiation, respectively. IL-1, produced by activated macrophages is an important mediator of the inflammatory response. TNF-α, IL-17, IL-22, and IL-26 stimulate keratinocyte production of cytokines, chemokines, and adhesion molecules, which, in turn, attract neutrophils and T lymphocytes, leading to amplification of inflammation. Blocking targets of the new biologics are IL-23 (tildrakizumab and guselkumab), IL-17 (secukinumab and ixekizumab), and IL-17 receptor (brodalumab). Blocking targets of the small molecules are phosphodiesterase 4 (apremilast) and JAK (tofacitinib and ruxolitinib). Source: Adapted from Kofoed K, Skov L, Zachariae C. New drugs and treatment targets in psoriasis. Acta Derm Venereol. 2014;95(2):133-139.
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