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PSO14-C010a(2) / July 2016

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The psoriasis immunological pathway

Prescribing information can be found by clicking on the 'Prescribing Information' tab when scrolling through the animation.

PSO14-C010a(2) / July 2016

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What is psoriasis?
Disease initiation

Pro-inflamatory cytokines released by keratinocytes activate the innate and adaptive immune systems

TNF-α inhibitors act here They bind to TNF-α preventing TNF-α from activating the innate and adaptive immune systems

TNF-α
IL-6
IL-1β
Antibody
Antibody
Antibody

Adaptive immune system

Innate immune system

Inactive macrophages

Inactive
mast cells

Inactive neutrophils

Inactive innate lymphoid cells

Active macrophages

Active mast cells

Active neutrophils

Active innate lymphoid cells

Cytokines released from activated dendritic cells stimulate T cells to differentiate

IL-12/23 inhibitors act here They bind to IL-12 and IL-23 preventing IL-12/23 from activating naïve T cells

IL-12
IL-23
Antibody

Th17

Th17

Th17 cells are present in higher numbers and expression of IL-17 is higher in psoriatic lesions compared with healthy tissue. Global gene expression studies have consistently demonstrated the upregulation of the IL-17 pathway in psoriasis.

Th1

Th1

It has been recognised for many years that the Th1 pathway is involved in psoriasis, although recent research has highlighted the significance of other pathways such as Th17.

Activated T cells and innate immune system cells release more cytokines which activate keratinocytes

IL-17A inhibitor Cosentyx (secukinumab) acts here It binds to IL-17A and prevents IL-17A from activating keratinocytes

TNF-α
IFN-γ
IL-17A
IL-17F
IL-22
Cosentyx
Cosentyx
Cosentyx
TNF-α
IFN-γ
IL-17A
IL-17F
IL-22

Keratinocytes are activated, proliferate and the cycle starts again

The psoriasis inflammatory cycle

Full Pathway
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PSO14-C010a(2) / July 2016

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