"The answer to your question about the purpose of Immunoglobulin E (IgE) is gradually emerging from a combination of human and animal studies.
"Humans make very high levels of IgE in response to infection by various parasites, including Schistosoma and Nippostrongylus brasiliensis. In the absence of IgE, or cells bearing the specific receptors for IgE (known as Fc receptors), these infections are considerably worse, and can be life-threatening or even life-taking. IgE also appears to play a role in resisting ticks of the Ixodid family, which carry among other diseases the organisms for Lyme disease and erlichiosis. But the exact workings of IgE remain far from fully understood."
Andrzej Szczeklik, chairman of the department of medicine at the Jagiellonian University School of Medicine in Krakow, Poland, adds his perspective:
"Immunoglobulin E (IgE) plays a key role in allergy. As a result, its other functions have received little attention. I would like to point out two little-appreciated, IgE-related phenomena that might be of benefit to humans:
"1) Atopics--that is, persons who produce too much IgE--have a mild hemostatic imbalance, meaning that their blood takes longer than usual to clot (roughly one fifth of Europeans and North Americans are atopics). Therefore, the bleeding time among atopics is slightly, but significantly, prolonged; the imbalance also reduces the stickiness of the blood platelets and delays the generation of thrombin, the key enzyme for coagulation. These phenomena might be relevant in the dangerous situations triggered by blood clotting in the arteries: a sudden cardiac arrest precipitated by coronary thrombosis (blockade of vessels that provide blood to the heart muscle) is a good example. In a recent study of 385 patients who had heart attacks, sudden cardiac arrest was far less common among the patients who entered the hospital with high serum IgE levels than among those whose IgE was not elevated. It therefore seems possible that high IgE, by depressing blood clotting, protect atopics against sudden cardiac arrest.
"2) Tissue injury characteristically results in a marked, transient rise in IgE levels in the blood. This phenomenon has been observed following heart attacks, surgery, burns, pulmonary thromboembolism and major trauma. Hence, IgE seems to be a part of the mechanism involved in acute-phase response. IgE might modulate the response to tissue injury through its powerful interaction with the cells of the immune system, such as mast cells, macrophages and eosinophils. Such hypotheses need further experimental verification, however.