Eczema (atopic dermatitis) and psoriasis are long-term, relapsing conditions characterized by visible skin inflammation. While eczema typically causes intense itching and red, dry patches, psoriasis results in thick, scaly plaques. Both are fundamentally diseases of immune system dysregulation, caused by a complex interplay between genetics and environmental influences. Although both manifest on the skin, the specific biological pathways driving the inflammation are largely distinct.
Primary Causes of Eczema
The primary driver of atopic dermatitis is the “outside-in” theory, centering on a defect in the skin barrier function. Genetic susceptibility, often involving mutations in the Filaggrin (FLG) gene, impairs the skin’s ability to retain moisture and act as a protective shield. Filaggrin is a protein essential for forming the outer layer of skin and its natural moisturizing factors.
A compromised skin barrier allows environmental allergens, irritants, and microbes to penetrate the skin easily. This penetration activates the immune system, leading to a chronic inflammatory response dominated by T-helper type 2 (Th2) cells. These Th2 cells release specific signaling proteins, such as Interleukin-4 (IL-4) and Interleukin-13 (IL-13), which drive the characteristic inflammation and intense itching of eczema.
This Type 2 inflammation promotes the production of high levels of immunoglobulin E (IgE) antibodies, which are strongly associated with allergic reactions. The ongoing inflammation further exacerbates the initial barrier defect by reducing the production of structural proteins like filaggrin. This creates a vicious cycle of damage and immune response, making the skin prone to water loss and vulnerable to triggers.
Primary Causes of Psoriasis
Psoriasis is primarily an immune-driven disorder, often classified as an autoimmune-mediated condition. This process is orchestrated by T-helper type 1 (Th1) and, more significantly, T-helper type 17 (Th17) cells.
The activation of this pathway begins with immune cells in the skin releasing Interleukin-23 (IL-23), which acts as a master switch that stimulates the survival and proliferation of Th17 cells. These Th17 cells then release potent inflammatory cytokines, most notably Interleukin-17A (IL-17A) and Interleukin-22 (IL-22).
The elevated levels of IL-17A and IL-22 act directly on the skin cells, called keratinocytes, causing them to mature and multiply at an accelerated rate. In healthy skin, a keratinocyte takes about 28 days to turnover, but in psoriasis, this process is reduced to days. This rapid, uncontrolled proliferation leads to the hallmark symptom: the formation of thick, raised, and silvery-scaly plaques.
The Underlying Genetic and Inflammatory Connection
Both eczema and psoriasis are rooted in polygenic inheritance, meaning multiple genes contribute to an individual’s susceptibility. Although the diseases have distinct primary pathways, they share the foundational requirement of a genetic predisposition interacting with environmental factors. Research has identified different major susceptibility genes for each condition, such as FLG mutations for eczema and a strong association with the HLA-Cw\0602 gene variant for psoriasis.
Despite these differences, both conditions are expressions of chronic, systemic inflammation driven by a dysfunctional immune system. This immune malfunction is the unifying factor, even though the specific T-cell populations that dominate the inflammation are different (eczema is Th2-driven and psoriasis is Th17-driven). The inflammatory signals generated in both diseases can extend beyond the skin, linking them to an increased risk of other systemic health issues.
External Factors That Trigger Flares
While genetics and internal immune pathways are the underlying causes, external factors act as triggers that provoke or worsen flare-ups. For psoriasis, a common infectious trigger is a streptococcal infection, such as strep throat, which frequently precedes the onset of guttate psoriasis. Physical injury to the skin, known as the Koebner phenomenon (e.g., a scratch, bug bite, or sunburn), can also cause new psoriatic lesions to appear in the affected area.
For eczema, exposure to environmental irritants and allergens is a major factor in exacerbating symptoms.
Common Triggers
- Harsh soaps, detergents, and fragrances.
- Airborne allergens like pollen and dust mites, which exploit the compromised skin barrier.
- Psychological stress.
- Significant changes in climate, such as very dry or cold weather.
These factors can disrupt the skin’s balance and provoke flares in both conditions.