Concepts:

1. Increased T-cell activity in response to various antigens.
    
2. Excess stimulation of T-cells by genetically altered ‘atopic” Langerhans cells. Langerhans cells are resident in the epidermis and are responsible for presenting antigens to lymphocytes.
    
3. Genetic defect in the epidermal barrier that makes the skin susceptible to breakdown by irritants such as detergents and dust mites. which may allow increased penetration of antigens.
   
   

exema - The Following Changes Have Been Observed:

1. The serum IgE levels are elevated. IgE are immunoglobulins that are produced in response to antigens or allergens and can themselves be measured and used as a marker of allergic type conditions Several genes have been associated with increased production of IgE. These levels are often related to the severity of the exema. However, 20% of atopics exema have normal or low levels.
    
2. There is a reduction in the cell-mediated immune response; chemotaxis of neutrophils and monocytes is reduced. These two last effects explain, the increased risk of infection of the skin in this condition.
    
3. It would appear that there is excessive stimulation of T cells which in turn increases the production of IL-4 (interleukin 4). Elevation of IL-4 and IL-13 may inhibit the antimicrobial – peptide gene expression which is part of the protective shield allowing proliferation of Staphylococcus aureus on and within the surface keratinocytes.
   
   There is also an increase in Langerhans cells in the epidermis. These usually present antigens to the immune system. Macrophages in this condition increase the production of IL-10 which, in turn, stimulates TH2 cytokine response. The fundamental cause is still elusive. There is a relative immune deficiency in the skin producing an increased risk of secondary infection.
    
4. A reduction in the barrier function of the epidermis is likely genetic which increases water loss and subsequent dryness of the skin.