These immune cells are present at numerous places in the body such as the skin, the digestive tract and the airways. “If the allergic patient comes into contact with the same allergen again, the mast cells release a series of mediators such as histamine and prostaglandins, which are responsible for the allergic symptoms", the researcher continues.  While the mechanisms associated with allergic reactions have been studied extensively and are well known, one fundamental question is yet to be answered: why has this type of reaction and, more precisely, the production of IgE been preserved over the course of evolution? “We still don’t know why these antibodies, which make us ill and can even cause death in extreme cases, have persisted over the course of evolution”, Thomas Marichal stresses.

Spotlight on allergies to venom

Thomas Marichal did his doctoral thesis while working in Fabrice Bureau’s team, in the GIGA Cellular and Molecular Physiology Research Unit. “Our objective was to understand which signals can initiate a type 2 reaction”, the young researcher explains. “And we made a major discovery since we were able to show that tissue damage was inducing the release of danger signals that were then detected by the immune system as powerful triggers of a type 2 response”, reveals Thomas Marichal. It was following this discovery, and within the framework of his work at Stanford University, that the scientist was particularly interested in the effect of certain venoms, especially those of the honeybee and a specie of viper. “We know that venom can induce a toxic response responsible for tissue damage while also being capable of causing an allergic reaction, as it is the case with people allergic to bees for instance”, continues the researcher. As for any other allergen, someone who has developed IgE against bee venom following an initial sting can be subject to a potentially fatal allergic reaction if they are stung again. “We attempted to reproduce this in laboratory animals which were injected with physiological amounts of venom”, Thomas Marichal points out. “We observed that mice resisted quite well to the initial amount of venom, even though it did cause tissue damage, a Th2 response as well as the production of IgE in the majority of them”, he adds. The scientists then exposed the mice that had developed IgE to a dose of bee venom, expecting them to develop an allergic reaction to the venom. Surprisingly, these animals were doing better than those that hadn’t developed antibodies against the venom. “Their temperature didn’t go down as much and they were able to survive better to a high dose of venom”, Thomas Marichal points out. In this case, the Th2 responses therefore seem to have a protective effect against bee venom rather than a noxious effect as in the case of allergies.