Atopy is defined by the tendency of an individual to produce IgE in response to low levels of a specific allergen which typically lead to development of diseases such as asthma, rhinitis or eczema. However, allergy phenotype manifestation depends on the interaction of two important factors, genetic factors and exposure to environmental allergens. The immune system is didactically divided into innate immunity, fast-acting immune response which existed before the pathogen installation and adaptive immunity, which has a specific response and immunological memory. The main cell that is involved in the communication between innate and adaptive immunity is the dendritic cell (DC) whose role is to capture, process and present the antigen, being then known as antigen-presenting cell (APC). Immature DCs capture the antigen and migrate from tissue to peripheral lymphoid organ where they differentiate into mature DC and present the antigen to naive T lymphocytes. Thus, naive T cells may differentiate into effector lymphocytes subtype (T helper lymphocytes - Th) as Th1 and Th2 lymphocytes. Another mechanism of immunity is involved in adaptive immunity is the humoral immune response and are represented by B lymphocytes and its products, mainly antibodies and acts against extracellular microorganisms and their toxins. Antibodies or immunoglobulins are soluble proteins produced by activated B lymphocytes known as plasma cells in response to antigens. The adaptive immune system comprises five immunoglobulin classes: IgG, IgM, IgD, IgE and IgA. Soluble allergens from dust mites as house dust mite, are the main factors that lead to the pathophysiological process of allergic inflammation. So have serious biological actions depending on the individual can contribute to the development of allergic reactions and result in severe clinical manifestations. In view of evidence that demonstrate the interaction of DCs with antibodies, we propose to investigate their influence on the presentation of the major allergens from house dust and the possible modulation of the immune response in atopic and non-atopic individuals.
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