Levels of cytokines such as interleukin 4 (IL-4) influence the effects the immune system has on the dermal barrier. IL-4 plays a role in T-helper cell proliferation and in stimulating B-cell activation, and can suppress production of filaggrin and similar proteins.7

While atopic dermatitis is particularly characterised by an immune response regulated by type-2 T-helper cells (Th2), Th2 activation is seen in non-atopic eczema such as discoid eczema and pompholyx. Th2 cells are involved in the allergic/inflammatory pathway reactions in the skin, stimulating mast cells to release histamine, and eosinophils.5

Of note, cytokines, including IL-2, IL4, and IL-13 inhibit the induction of an adequate immune response in epithelial cells, which is seen in the reduced levels of antimicrobial peptides in eczematous skin. A potential consequence of this is the increased likelihood of Staphylococcus aureus colonisation of the skin, which is typically found in people with atopic dermatitis.

Other dermal flora changes in eczema include risk of increased levels of the yeast Malassezia furfur (formerly called Pityrosporum ovale or orbiculare) or the Molluscum contagiosum virus. Reduced resistance to dermal infection is a factor in why herpes simplex can be much more serious for someone with atopic dermatitis.5