Eczema (atopic dermatitis) and asthma involve a dysregulated immune system, but they are not classified as classical autoimmune diseases. Both are categorized as chronic inflammatory conditions that fall under the umbrella of atopic disorders. This distinction is based on the immune response targeting external environmental factors rather than the body’s own healthy cells. Confusion often arises because the underlying inflammation uses many of the same immune pathways active in autoimmune disorders.
Distinguishing Autoimmunity from Atopic Disorders
Autoimmunity is an immune response where the body’s defense mechanisms mistakenly attack and destroy its own healthy tissues. In true autoimmune diseases (e.g., Type 1 diabetes or rheumatoid arthritis), the immune system targets specific proteins or cells, leading to tissue damage. This represents a failure of immune tolerance, meaning the body cannot distinguish between “self” and “non-self” components.
Atopic disorders, in contrast, are a hypersensitivity reaction to typically harmless substances known as allergens. These conditions involve an exaggerated immune response, often driven by Immunoglobulin E (IgE), directed at external triggers like pollen, dust mites, or certain foods. The resulting inflammation is a reaction to environmental exposure, not an attack on the body’s internal components. Both eczema and asthma are Type I hypersensitivity reactions, placing them firmly in the atopic category.
The Immune Basis of Eczema (Atopic Dermatitis)
Eczema is driven by genetic predisposition and immune system overactivity. A foundational vulnerability is a compromised skin barrier, which acts as the body’s first line of defense. Genetic mutations, particularly in the filaggrin gene, can lead to a deficiency in proteins needed to maintain the skin’s structure and moisture.
This defective barrier allows environmental allergens and irritants to penetrate the skin, triggering an inflammatory cascade. The immune system responds with a Type 2 inflammatory profile, characterized by the activation of T-helper 2 (Th2) cells. These cells release cytokines, including Interleukin-4 (IL-4) and Interleukin-13 (IL-13).
IL-4 and IL-13 perpetuate inflammation and further impair the skin barrier function, leading to the characteristic dry, itchy, and inflamed patches. This Th2-driven response also stimulates B-cells to produce excessive IgE antibodies, which become sensitized to environmental allergens. The presence of allergen-specific IgE molecules is a hallmark of atopy, differentiating this hypersensitivity from an autoimmune attack.
The Immune Basis of Asthma
Asthma is characterized by chronic inflammation of the airways and bronchial hyperresponsiveness—an excessive tendency for the airways to narrow. Similar to eczema, the most common form, allergic asthma, is rooted in a Type 2 hypersensitivity response to inhaled allergens. When an atopic individual inhales an allergen, the immune system mounts a response involving IgE antibodies already bound to mast cells lining the airways.
Upon re-exposure, the allergen binds to the IgE on these mast cells, causing them to rapidly release inflammatory mediators like histamine. This initial reaction causes acute symptoms such as bronchospasm and wheezing. The chronic phase is maintained by Th2 cells, which release cytokines such as IL-5.
Interleukin-5 promotes the growth and activation of eosinophils, a white blood cell that accumulates in the lungs. Eosinophils contribute significantly to persistent airway inflammation and tissue remodeling. This persistent, IgE-mediated, and eosinophil-rich inflammation defines the allergic nature of asthma, which reacts to external triggers rather than internal self-attack.
The Atopic March: Understanding the Shared Link
The frequent co-occurrence of eczema and asthma, along with other allergic conditions like hay fever (allergic rhinitis), is formalized by the concept known as the “Atopic March.” This describes a typical chronological progression of atopic diseases that often begins in infancy and continues into childhood and adolescence. Infants may first develop eczema, which then serves as a risk factor for the subsequent development of food allergies, allergic rhinitis, and finally asthma.
This sequence is linked by a shared genetic susceptibility to atopy and the common mechanism of Type 2 inflammation. The initial skin barrier defect in eczema may be a key driver, allowing environmental and food allergens to enter the body through the skin and sensitize the immune system. This sensitization through the impaired skin can then predispose the individual to develop allergic responses in other organs, such as the lungs and nasal passages.
Severity of eczema early in life predicts progression along the Atopic March. Those experiencing more severe atopic dermatitis have a significantly higher likelihood of developing asthma later. This interconnectedness highlights that while eczema and asthma are distinct conditions, they share a common underlying predisposition to generate hypersensitivity reactions to the external world.