Figure 3.

The possible implications for β-defensins in atopic dermatitis. Atopic dermatitis (AD) is a chronic, relapsing disease associated with itchy lesions on the skin, across a large proportion of the body. These lesions are characterised by a breakdown in the barrier function of the uppermost regions of the skin (the epidermis). This allows for an increase in bacterial infection, which is made worse by bacterial production of proteases that further breakdown the junctions between cells, as is the case for V8 (SspA) production by Staphylococcus aureus. In AD, there is a downregulation in a number of Th1-associated cytokines, such as Tumour Necrosis Factor (TNF)α and interleukin (IL)-1β, as well as antimicrobial peptides, such as the β-defensins (including HBD2). It is thought that the AD-associated, localised cytokine milieu, which has a T helper (Th)2-skewed phenotype, is responsible for this reduction. Inhibition of the induction of β-defensins prevents proper bacterial removal/inhibition, worsening infection and AD pathology. Abbreviations: interleukin (IL), Toll Like Receptor (TLR), pathogen recognition receptor (PRR).