Our immune system does a remarkable job of protecting us against the harmful effects of infectious agents that cause disease. However, every so often this defence mechanism can be made to turn on itself, triggering a violent, often fatal reaction against its host. Understanding how the immune system can be prompted to behave in such a self-destructive manner can be traced to discoveries made by this year’s Nobel Laureate in Physiology or Medicine.

Through a series of experiments, Charles Richet demonstrated that this adverse response, which he termed anaphylaxis, was far from being an accident or an aberration, as many scientists in the field had thought. Working with Paul Portier, Richet discovered that dogs that had received an injection of sea-anemone poison without any noticeable distress always went into shock and died quickly after receiving a weaker dose a set amount of days later. Instead of raising tolerance towards the toxin, as expected, the initial dose in fact made animals highly sensitive for a set period of time to even miniscule amounts of the poison. Systematically administering a number of poisons in this manner and examining the violent reactions led Richet to conclude that anaphylaxis behaves in a similar, but opposite, manner to immunity. For instance, reactions were specific to the poison in question, and transferring blood from an affected animal to a healthy one could provoke hypersensitivity to the toxin.

Identifying the principal triggers for anaphylaxis and the early, alarming symptoms led to the creation of a valuable medical warning system. Physicians could now identify patients who might be sensitive to treatments for infectious diseases that contain toxins from bacteria, such as diphtheria. More recently, this adverse immune response has become the object of intense scrutiny in completely different area. Anaphylaxis is thought to be the cause of adverse reactions that a small number of individuals have towards certain proteins found in food.