Anaphylaxis is a potentially life-threatening, rapidly progressing systemic hypersensitivity reaction that can result in death. Because it can be triggered within minutes after antigen exposure (eg. certain foods, insect stings, drugs) and is associated with serious cardiovascular problems and airway obstruction, anaphylaxis can be considered the most aberrant example of incorrect immune response and destroyed immune balance. The key players in anaphylaxis are considered to be mast cells and basophils, which share a few distinct features, such as expression of FcεRI receptor that binds IgE with high affinity and the ability to rapidly degranulate. Mast cells are already well-known as the major effector cells during a classical mechanism called IgE-dependent anaphylaxis, whereas the important and specific role for basophils and their migration occurring during anaphylaxis was described only recently. Distinct mechanisms, triggers, features of anaphylactic reactions, clinical symptoms and arising specific roles of a single effector cell reflect high complexity of anaphylaxis and consequently the difficulties with its understanding. This thesis overviews existing studies on mentioned topic and defines mechanisms of action concerning anaphylaxis.
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