ABSTRACT
A key element of both asthma and atopic dermatitis is the development and activation of Th2 cells, a subset of T-helper cells that initiates and maintains local tissue inflammation. Researchers and clinicians have together classified two forms of atopic dermatitis: intrinsic and extrinsic. A number of theories have been offered to explain the large geographic variations in the prevalence of asthma, allergic rhinoconjunctivitis, and atopic eczema. In many cases atopic dermatitis predates the development of asthma and allergic rhinitis, suggesting that it is the first step in the development of subsequent allergic diseases. The characteristic skin lesions of atopic dermatitis result from the disturbed cellular immunity. Immunoglobulin E (IgE)-mediated autoreactivity contributes to the defective tolerance of atopic dermatitis patients and can appear very early to contribute to disease flares. Eczema flares in patients with extrinsic atopic dermatitis are exacerbated by aeroallergens and foods, as reflected by elevated levels of antigen-specific IgE to these substances.
