Yes, eczema is an inflammatory disease. Atopic dermatitis, the most common form of eczema, is driven by an overactive immune response that causes chronic inflammation in the skin. It affects 10% to 20% of children and 2% to 10% of adults worldwide, making it one of the most prevalent inflammatory conditions in humans.
Why Eczema Is Classified as Inflammatory
Eczema isn’t simply dry or irritated skin. It’s a condition where the immune system mounts an exaggerated response, flooding the skin with inflammatory cells and chemical signals that cause redness, swelling, and itching. The central players are a type of immune cell called Th2 cells, which release signaling molecules (particularly IL-4 and IL-13) that ramp up inflammation and trigger the production of IgE, an antibody associated with allergic reactions.
This inflammatory cascade also recruits other immune cells, including eosinophils, mast cells, and basophils. Damaged skin cells release their own alarm signals that amplify the response further. The result is a self-reinforcing loop: inflammation damages the skin barrier, which lets in more irritants and allergens, which triggers more inflammation.
The Skin Barrier Connection
There are two leading theories about what starts this cycle. The first points to the immune system itself malfunctioning, with the Th2-driven inflammation coming first and weakening the skin barrier as a consequence. The second points to a barrier defect as the trigger, particularly mutations in a protein called filaggrin that helps hold the outer layer of skin together.
People with filaggrin mutations have a more porous skin surface. Allergens and proteins that would normally stay outside the body can slip through, provoking an outsized immune response. Research published in the Journal of Allergy and Clinical Immunology found that this barrier defect doesn’t just cause local skin inflammation. It can drive allergic responses at distant sites in the body, like the airways, because antigens penetrating the skin enter the bloodstream and activate immune cells systemically. This helps explain why many people with eczema also develop asthma or hay fever.
How Inflammation Changes Over Time
The type of inflammation in eczema shifts depending on whether you’re dealing with a fresh flare or a long-standing patch.
During an acute flare, fluid collects between skin cells, creating the tiny blisters and weeping that many people recognize. Under a microscope, the skin is swollen with fluid and packed with immune cells, particularly lymphocytes and eosinophils. The outer layer of skin stays relatively normal in structure but becomes waterlogged from the inflammatory response underneath.
In chronic eczema, the picture looks different. The skin thickens significantly, building up extra layers of cells in a process similar to what happens in psoriasis. The deeper layers develop scar-like tissue. The dramatic fluid swelling of acute flares fades, replaced by a drier, tougher, leathery texture. The immune profile shifts too: while acute eczema is dominated by Th2 cells, chronic lesions show a rise in Th1 and Th17 cells, broadening the inflammatory response beyond its original allergic character.
Measuring Inflammation in Eczema
Because eczema is fundamentally inflammatory, doctors can track its severity through blood markers. A review by the International Eczema Council found that a molecule called CCL17 (also known as TARC) has the strongest correlation with how severe eczema is at any given time. It works as a homing signal that attracts Th2 cells into the skin, and its levels in the blood rise and fall in step with flare severity.
Other measurable markers include IgE levels, eosinophil counts, and several other signaling molecules tied to the Th2 immune pathway. These biomarkers aren’t typically used for initial diagnosis, which is based on clinical appearance and history, but they help gauge how active the underlying inflammation is, especially in moderate to severe cases where treatment decisions hinge on that information.
Treatments That Target Inflammation
Because eczema is inflammatory at its core, effective treatments work by suppressing or redirecting that immune response rather than simply moisturizing the skin.
The foundation of management includes moisturizers to support the skin barrier alongside topical anti-inflammatory treatments. Topical corticosteroids remain a mainstay, calming local inflammation during flares. Newer topical options include calcineurin inhibitors, which block immune activation in the skin, and several recently approved creams that target specific inflammatory enzymes.
For moderate to severe eczema that doesn’t respond to topical treatments, a newer class of injectable medications called biologics has changed the landscape. These drugs are designed to block the exact inflammatory molecules driving eczema. Dupilumab, for example, blocks IL-4 and IL-13, the two key Th2 cytokines. Newer biologics target IL-13 alone or block the itch-specific signaling molecule IL-31.
The most recent additions are oral JAK inhibitors, which work by intercepting signals inside immune cells before inflammatory molecules are even produced. Two, abrocitinib and upadacitinib, have FDA approval. They broadly block many of the cytokines involved in eczema, including IL-4, IL-5, IL-13, and IL-31, which is why they can produce rapid improvement in both itch and skin clearance. The American Academy of Dermatology’s most recent guidelines strongly recommend these options alongside biologics for patients with significant disease.
One notable recommendation in those same guidelines: systemic corticosteroids (oral steroids like prednisone) are strongly recommended against. While they suppress inflammation powerfully in the short term, they cause rebound flares when stopped and carry serious side effects with repeated use. The shift toward targeted therapies reflects a deeper understanding of eczema’s specific inflammatory pathways, allowing treatments that dampen the right parts of the immune system without broadly suppressing it.