Our understanding of eczema (also known as atopic dermatitis) has advanced significantly in recent years — including how the skin barrier, immune system, microbiome and neuro-immune pathways contribute. Eczema (atopic dermatitis) affects millions worldwide and is more than simply dry or itchy skin; it is an inflammatory condition with complex and interrelated causes.
Although most commonly diagnosed in childhood, eczema also affects many adults, including significant numbers aged over 60. The growing burden of eczema in high-income, urbanised nations may reflect the influence of modern environments and lifestyles, where factors such as pollution, reduced microbial exposure and chronic stress are increasingly recognised as contributors to disease onset and persistence.
Eczema remains a chronic and multifaceted condition, influenced not only by genetics and immune responses but also by environmental interactions that extend beyond the skin barrier, shaping how we understand, prevent and treat it. At its core, eczema is shaped by dynamic feedback loops between the skin, immune system, nervous system, and environment. These systems continually influence one another, driving inflammation, itch, barrier disruption, and disease flares. This interconnectedness makes eczema difficult to manage and highlights the importance of studying it in human-relevant systems.
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Impacts on quality of life
Beyond its physical symptoms, eczema has a substantial impact on quality of life. Chronic itch, visible inflammation, sleep disruption and the psychological burden of a condition that often fluctuates unpredictably all contribute to its daily toll on patients.
Eczema is closely linked to other atopic conditions, particularly food and respiratory allergies through shared genetic, immune and barrier mechanisms that can predispose individuals to multiple allergic diseases across their lifetime.
In addition, recurrent infections and flare-ups can add to the daily burden of eczema, compounding its effects on sleep, comfort and overall wellbeing.
The skin barrier: first line of defence
The outermost layer of the skin forms a dynamic barrier that protects against irritants, allergens and microbial invasion while preventing excess water loss. A key component of this defence is filaggrin, a structural protein that helps bind skin cells together and maintain hydration within the stratum corneum.
When barrier integrity is compromised, for example through filaggrin deficiency, genetic variation or chronic inflammation, the skin becomes more permeable. Allergens and microbes can enter more easily, while vital moisture escapes, setting off inflammatory cascades that lead to the itch–scratch cycle so characteristic of eczema. This disruption not only drives flares – but also increases vulnerability to bacterial and viral infections, as seen in conditions such as eczema herpeticum and molluscum contagiosum, highlighting how essential an intact barrier is to overall skin health.
The weakened skin barrier in atopic dermatitis does not just lead to dryness and inflammation; it also increases susceptibility to infection, particularly in moderate-to-severe cases. People with eczema are more prone to bacterial colonisation and viral infections, underscoring the skin’s vital role as an immune and physical barrier.
When the barrier breaks down
Once the skin barrier is breached, the immune system responds rapidly and sometimes excessively. Antigens that would normally be kept out now penetrate the skin, triggering activation of type-2 immune pathways and the release of cytokines such as IL-4, IL-13 and IL-31. These signalling molecules drive inflammation, impair barrier repair, and intensify itch, reinforcing the itch-scratch cycle that is central to eczema pathology.
This self-perpetuating cycle not only sustains inflammation but further weakens the barrier, increasing sensitivity to environmental triggers and prolonging disease flares. Recent advances in biologic therapies have focused on interrupting these pathways, targeting specific cytokines or their receptors to reduce inflammation, relieve itch and help restore the skin’s natural homeostasis.
A condition shaped by many influences
Eczema does not arise from a single cause but from a complex interplay of genetic susceptibility, environmental exposures and microbial imbalance. Genetic variation, particularly in barrier or immune-related genes such as FLG, can increase susceptibility, while environmental triggers including pollutants, detergents and allergens often influence when and how flares occur.
Research into the skin microbiome has added another important dimension to our understanding. Disruptions in microbial diversity, especially overgrowth of Staphylococcus aureus, can exacerbate inflammation and delay healing. These findings highlight eczema as a condition driven by continuous interactions between the skin, immune system, microbes, and environment.
Together, these insights are reshaping how we think about eczema—shifting the focus from managing flares alone toward strategies that address underlying drivers of disease activity.
Early intervention and barrier support
Although genetics play a key role in atopic dermatitis, it is increasingly recognised that strengthening the skin barrier early in life may help to reduce risk or delay onset, particularly in infants with a family history of eczema. One such approach is the regular use of emollients from birth that aims to protect the developing skin barrier and maintain hydration. While results have been mixed, these studies underscore the importance of early barrier protection. Other strategies that focus on prevention include reducing exposure to environmental triggers such as harsh detergents or extremes of humidity and supporting microbial diversity through balanced hygiene and diet. No single approach has yet proven universally effective, but collectively these approaches underline the central role of the skin barrier in eczema risk and progression.
Understanding how genetic predisposition, environmental exposure and skin barrier development interact remains central to developing truly preventive strategies and highlights the need for human-relevant models that can capture these complex interactions.
Treatments and new directions
Management of eczema has progressed significantly in recent years. Traditional approaches, including emollients and topical corticosteroids that focus on symptom relief, remain central to symptom control, while targeted biologics and JAK inhibitors now offer effective options for many with moderate-to-severe disease by acting on specific immune pathways. These advances have transformed outcomes for patients whose eczema was previously difficult to manage. The therapeutic pipleline of novel systemic and topical therapeutics is deep and strong with many assests now in clinical development programs. Patients and their healthcare professionals can look forward to increased options in coming years.
At the same time, research continues to explore complementary strategies focussed on barrier repair, microbiome support and personalised approaches that account for individual genetic and environmental factors. There is also growing interest in early intervention, particularly in childhood, with evidence suggesting that protecting the skin barrier and managing inflammation early in life may influence the long-term course of the disease.
Together, these developments reflect a growing understanding of eczema as a systemic condition rooted in the interplay between the skin, the immune system and the environment.
Looking ahead
Eczema research has advanced rapidly, from recognising the importance of the skin barrier to mapping the immune pathways that drive inflammation and itch. Yet, important questions remain about how genetic predisposition, environmental exposure and microbial factors interact to shape disease onset, severity and persistence.
Addressing these challenges will depend on research models that reflect the complexity of human skin, enabling researchers to study barrier function, immune responses and treatment effects in a physiologically relevant context. By deepening our understanding of these interactions, the field moves closer to not only improved treatments, but to strategies that may ultimately prevent eczema and restore long-term skin health.
About the author
Professor Alan Irvine is a Consultant Dermatologist at St James’s Hospital/Children’s Health Ireland and Professor of Dermatology at Trinity College Dublin. A recognised authority in epithelial genetics and inflammatory skin disease. Professor Irvine’s work has helped shape our understanding of atopic dermatitis and the skin barrier.
January 2026
