IL-22 upregulation characterizes atopic dermatitis lesions. However, blocking IL-22 has not been defined in human subjects. A recent study sought to evaluate the cellular and molecular effects of fezakinumab (anti-IL-22) versus placebo taken from biopsy specimens.
Atopic dermatitis is the most common chronic inflammatory skin disease with increasing prevalence. IL-4 and IL-13 are the 2 lead cytokines that are upregulated in atopic dermatitis and they are inhibited through Dupilumab (Dupixent)
However, not every patient responds successfully and there are other pathways that may play a role in atopic dermatitis. IL-22 has been postulated to be a main driver of epidermal hyperplasia and barrier defects. IL-22 might be central to atopic dermatitis pathogenesis. Fezakinumab has shown significant clinical improvements in patients with severe eczema disease. Conclusions of the study showed:
- Significant improvement in the cutaneous gene signature with fezakinumab was only present in patients with high baseline IL-22 skin expression but not in those with low baseline IL-22 expression.
- Downregulation of multiple immune pathways with fezakinumab was restricted to the IL-22 high group.
The study suggests the potential for personalized medicine in patients with atopic dermatitis. The baseline expression of IL-22 may guide the therapy of an inhibitor such as fezakinumab.
Pharmaceutical medication is changing now and no longer the “one size fits all” approach is being used. Diseases such as atopic dermatitis have different causes/triggers and a single medication may not be right for everyone. We are seeing this currently in asthma where there are biologic medications for those who have IgE asthma (Xolair) or eosinophilic asthma (Nucala, Fasenra,Cinqair).
It is soon to tell if Fezakinumab will work for patients with eczema, but it seems to work in a particular subset of those patients. As of now, the only biologic medication approved is Dupixent, otherwise mostly topical creams and conservative care are used to treat this condition.