Topical corticosteroids (TCS) remain the first-line treatment for (AD). This narrative review examines clinical data on the immunomodulatory effects of TCS and recent treatments for atopic dermatitis (AD) in early childhood in the context of atopic comorbidities. While TCS are effective in reducing several markers of inflammation in infants with AD, certain type 2 cytokines, such as interleukin (IL)−4, IL-5, and IL-13, remain uncontrolled in the infant stratum corneum, a major source of dysregulated systemic cytokines. A pathomechanism known as remote priming has been identified, wherein allergen-induced antigen-specific immune responses in disrupted skin facilitate allergen-sensitizing immune responses in distant mucosal barrier sites, such as the gut or lung. In the gut, remote priming occurs through the activation of epidermal type 2 innate lymphoid cells (ILC2), which prime gut mast cells and promote food allergies. ILC2s produce IL-5 and IL-13, which remain present in the epidermis with TCS. Consequently, ILC2 cells in the skin of children with AD may remain able to contribute to remote gut priming. Type 2 cytokines also promote immunoglobulin E (IgE) production—a marker of atopic development in children. Over 16 weeks, children aged 6 months to 5 years treated with dupilumab and TCS show a 70% reduction in IgE levels, whereas those treated with TCS alone exhibit a 30% increase in IgE levels. These observations highlight the need for a more comprehensive approach to managing infant AD. Therapies that target inflammation originating from both innate and adaptive effector cells involved in type 2 inflammation may not only alleviate the burden of AD but also disrupt the progression of the atopic march.
Chau et al. (Tue,) studied this question.