Fig. 1.

A) For allergists, all allergic symptoms are centered around IgE antibodies. Its fixation via IgE receptors on effector cells means that an allergic person is sensitized. Upon subsequent allergen contact, the IgE gets crosslinked and mediators are released from the activated mast cells, causing inflammation and typical allergic symptoms. The mast cell mediators best known are tryptase, histamine, and leukotrienes, but also different cytokines, including tumor necrosis factor-alpha (TNF-α). B) Tumor cells do overexpress numerous antigens at a higher density and distinct composition than healthy cells. IgE bound to FcεRI can be crosslinked by overexpressed tumor antigens on malignant cells, resulting in activation of the effector cells, release of cytotoxic mediators and cytokines like TNF-α, and subsequent antibody-dependent cell mediated cytotoxicity (ADCC). Similarly, IgE via FcεRII (CD23) is involved in killing the tumor cells through antibody-dependent cell mediated phagocytosis (ADCP). It is possible that these mechanisms play an important role in cancer surveillance when the number of aberrant cells is still low. Consequently, a state of IgE deficiency is a risk for failure of this surveillance machinery.