Pathology and Therapeutic Response in Atopic Dermatitis

Can baseline blood markers of skin-barrier disruption help identify patients who are more likely to respond?

Atopic dermatitis (AD) is marked by a dysfunctional skin barrier and chronic itch, largely driven by cytokines such as IL-4 and IL-13 produced by keratinocytes. Scratching worsens skin barrier function and causes damage and perpetuate the itch–scratch cycle.

At the same time, type XXII collagen is found in the junction where the hair follicle attaches to the dermis, functioning as a cell adhesion ligand, linking the epithelial cells and fibroblasts to the extracellular matrix. This interaction allows the integrity of the tissue junction.

This is why we have investigated the biomarker PRO-C22 that precisely quantifies type XXII collagen in blood. We found that higher levels of PRO-C22:

• Correlate with itch severity

• Reflect treatment response to biological treatment
  

Our investigation has shown that the blood-based PRO-C22 biomarker can offer new insights into barrier-related pathology and therapeutic response in AD.