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In recent years, research has revealed important insights into the pathogenesis of the most common form of dermatitis, atopic (allergic) eczema, also known as atopic dermatitis. It is now understood that genes that control skin integrity (FGN) and immune responsiveness (IL-10) play a critical role in development of atopic eczema.
The gene FGN encodes a protein called filaggrin. Filaggrin binds to keratin intermediate filaments in the skin to form a protective waterproof layer on the surface of the skin that keeps out a wide range of substances that can be recognised by the immune system. Reduced activity of filaggrin results in the formation of holes in the skin, through which environmental substances such as pollens can readily penetrate, making it dry and often scaly .
Once environmental substances have penetrated the skin, those people whose immune system is able to produce an allergic-type of immune response develop an abnormal type of antibody against these environmental substances called IgE. The interaction between environmental substances and their corresponding IgE antibodies in the skin leads to development of a local inflammatory reaction causing atopic or allergic eczema/dermatitis. The protein produced by the gene IL-10 has been shown to suppress the production of IgE antibodies and inflammation .
Therefore, now that the two most important factors that are involved in development of atopic eczema/dermatitis are known, this SSHD-FGN/IL10 molecule targets and support both the genes FGN and IL-10.