Once animals began to diversify, a major trend was for some animals to parasitize others. Some animal parasites became wholly or largely committed to particular lineages of animal hosts, in which they subsequently diversified. Such lineage-specific parasites (some examples in Table 2 ) are another general factor expected to drive immunological novelty. These parasites often establish prolonged, intimate, and extensive infections in their chosen hosts that have profound fitness consequences such as castration or death (Lafferty and Kuris, 2009a) . Furthermore, given the phylogenetic diversity represented among these parasites, it is not surprising they would evolve novel methods of infectivity. For example, ichneumonid and braconid hymenopteran parasitoids have acquired mutualistic polydnaviruses that function to suppress the immune responsiveness of their hosts and facilitate parasitoid infection (Webb et al., 2009) . In contrast, without the aid of viral symbionts, larvae of digenetic trematodes secrete both anti-oxidants and immunosuppressive factors that down-regulate snail host immune components for a period sufficient to enable them to complete their lengthy period of larval development (Hanington et al., 2010a) . Therefore, the immune response devised by a particular host lineage afflicted with its own phylogenetically distinct, host specific, and harmful parasites would likely be divergent from the responses mounted by a different host group experiencing its own lineage-specific parasites (Figure 2) . This is not to imply that only animal parasites have developed lineage-specific associations with hosts, but merely serves to show that specialized parasites can help us understand the origins of immunological novelties.