Allergy either results from a pathological excessive immune reaction, or from the defective induction of tolerance to otherwise harmless antigens. Allergic reactions are mounted by mechanisms of innate and adaptive immunity. The development of an allergic response can be divided in sensitization and elicitation phases. Immediate type allergic reactions (e.g. anaphylaxis, urticaria, rhinoconjunctivitis allergica, allergic asthma) are mediated by IgE antibodies which are produced by B cells stimulated by allergen‐specific Th2 cells. Crosslinking of allergen‐specific IgE on membrane surfaces of mast cells and basophilic granulocytes leads to release of soluble mediators which may cause systemic symptoms within minutes to hours. The following infiltration of eosinophilic granulocytes and Th2 cells directs chronic inflammation.

Humoral cytotoxic immune reactions (e.g. drug induced cytopenia) are mediated by IgG and IgM antibodies which are directed against membrane associated antigens. IgG and IgM antibodies directed against soluble antigens elicit immune complex mediated cytotoxicity (e.g.drug induced vasculitis).Delayed type immune reactions (e.g.contact dermatitis) are based on the activation of antigen specific CD4⁺ and CD8⁺ T cells and need 24 h to 48 h to develop. Upon recurrent contact with identical antigens, recruitment of CD4⁺ and CD8⁺ T cells cause inflammation and cytotoxic induced apoptosis in target cells as well as cytokine mediated leukocyte infiltration. Subsequent immigration of CD4⁺ Th2 cells provides anti‐inflammatory mechanisms leading to resolution of the inflammatory response and tissue repair.