Introduction         

      Eczema is a hereditary, non-contagious autoimmune disease that causes extreme flare ups that results in a rash (1). When a person has eczema, they have a flare up due to an irritant that will be unique to them. Because the skin is a protective barrier from the external environment as a person scratches the skin opens allowing more allergen to enter (1). According to Peter Parham, eczema is common in families that have a history of asthma and will sometimes clear before becoming an adult (2). There are many different types of eczema that can result in a person having the symptoms that are related with eczema, and people may have more than one type which can complicate the treatment that they might receive (3).

         Atopic dermatitis the most common form that causes symptoms that include: dry skin, redness in the area of a flare up, itching, sores, and a rash. Patients that have Atopic dermatitis normally have dehydrated skin due to the water loss from the skin barrier being broken, and may have a lower pH which prevents the enzymes in the skin from functioning at their optimal level (1). People with defects in the filaggrin gene, which is responsible for formation of the stratum corneum boundary are more likely to form atopic dermatitis than those without the mutation (1). The mutation on the filaggrin gene result in loss-of-function which is why the stratum corneum is compromised and the skin is not as strong as it should be (1). The mutations that result in this loss-of-function are R501X and 2282de14 and they decrease the amount of filaggrin peptides that are available in the skin to form the proper stratum corneum (1).

        It has been found that regulation of the JAK-STAT pathway can be compromised in a patient with eczema (4). Multiple mutations in the pathway can lead to the formation of the higher levels of IgE in the body and that can result in the symptoms that are felt with a patient suffering from eczema, specifically atopic dermatitis (4). A specific defect is the removal of the suppressor of cytokine signaling 2 (SOCS2) which is responsible for negative feedback in the JAK-STAT pathway (4). The study done in a mouse showed that the defect in SOCS2 showed high levels of both IgE and the Th2 response with lower levels of IL-17 (4). IL-17 is shown to increase the activity of adhesion molecules in the skin, so by having lower levels of the IL-17 a person with atopic dermatitis may have a slower healing time when the skin is open or cracked (4). Eczema is also a common side effect of other autoimmune diseases. Many times, in eczema a person is having a TH2 response to an allergen that does not pose an actual threat to their life, and they have larger amounts of IgE in circulation (2). With high levels of IgE available in the blood stream when a person is exposed to their allergen the response can be quick because the IgE is already available to bind and release cytokines and histamine.