Interleukin 22

And that's kind of what we want to dive into a little bit next.

But so you have these TH-22 cells and, um, These Th22 cells secrete IL-22, which promotes keratinocyte hyperproliferation and abnormal epidermal thickening, and this can help produce that characteristic well-demarcated scaly plaque.

The key point here, though, is that the keratinocytes are not just passive targets of the inflammation.

Once stimulated, these keratinocytes will also release additional cytokines and chemokines that recruit and activate more T-cells, dendritic cells, and neutrophils.

So clinically, the most important pathway to remember is the IL-23, TH17, and IL-17 axis.

And the IL-23 is a cytokine that supports, they support the Th17 cells.

And then the IL-17 drives keratinocyte activation and neutrophil inflammation and downstream cytokines such as IL-22, which contribute to epidermal hyperplasia.

So that's a lot.

It binds to the IL-23 receptor on responsive immune cells.

That contributes to downstream signaling and the release of inflammatory mediators, including IL-17A, IL-17F, IL-19, and IL-22.

Those signals can drive abnormal activation and proliferation of keratinocytes, the major cells in the outer layer of the skin.

The visible result is thickened, inflamed, scaly plaque associated with psoriasis.