We develop the hypothesis that parasites do not invade extreme environments, i.e. hostile hosts, but rather ‘create’ them. We argue that parasites may have driven the evolution of the constitutive and adaptive immune system. This leads to several implications. First, parasites respond to ‘genes to kill’ by ‘genes to survive’ and this triggers an indefinite selection of measures and counter-measures. Second, these revolutionary arms races may lead to local adaptation, in which parasite populations perform better on local hosts. Third, the evolution of the immune system, whose responses are predictable, may allow parasites to specialize, to evade and even to manipulate. Finally we show that the correlations between the increase in the antibody repertoire, the expansion of MHC loci and parasite pressures support our hypothesis that both host complexity and parasite pressures can be invoked to explain the diversity of antibodies, T-receptors and MHC molecules.
