The previous two sections argue first that sym-bionts can actively contribute to resistance to natural enemies, and second that many of them will also interact with the immune system of the host. What are the consequences of these for immune system evolution? With respect to the former, the resistance functions provided by symbionts may alter selection pressures on the components of host immunity that they complement. If a dominant parasitoid natural enemy is resisted by symbiont infection, this may alter the pattern of selection on the host's own surveillance and response mechanisms. The requirement to maintain standing prophenoloxidase- and haemocyte-based defences may decline. Thus, the conjecture is that symbiont-induced natural enemy resistance is likely to be accompanied by changes to the host's input to standing defences. This may have ramifications for the success of parasites and pathogens of the host to which the symbiont does not provide protection. The extent to which this occurs will depend on the extent to which symbi-ont-mediated protection is independent of hosts, or driven through them. If it is a case of the symbionts potentiating existing systems, then selection for the removal of the host standing components will be weak or non-existent. If the symbiont effect is direct, however, host standing systems become redundant, and potentially subject to weakened selection for their maintenance.
The second issue raised in this chapter was the interaction between symbionts and the immune system of the host. The observation that symbionts can interact with host immune systems indicates we should ask whether symbionts have produced selection for immune systems that accommodate them? It is notable that the insect immune system, despite being classically considered 'generalist' in its action, still shows some evidence of being fast-evolving, both in terms of the strength of positive selection and the turnover of elements within the systems. The signature of positive selection is particularly strong in the signalling components of the humoral immune cascade (Begun and Whitley, 2000; Jiggins and Kim, 2007), although interestingly not in the receptors or the effectors (Jiggins and Hurst, 2003; Lazzaro and Clark, 2003), and is strong also in receptors associated with phagocytosis (Lazzaro, 2005).
Turnover of the genes comprising immunity occurs in subtly different compartments. It is particularly pronounced in the complement of AMPs, which, despite showing little evidence of positive selection, vary in constitution from species group to species group (Sackton et al., 2007). This observation implies that new AMP molecules are being recruited to kill bacteria and fungal enemies over evolutionary time, and, as importantly, other AMP molecules are being lost. The complement of receptors for phagocytosis similarly shows variation between species.
This signature of rapid evolution is not typical of a generalist system. Rather, it implies that the immune system faces common parties with which it interacts, as well as providing a generalist system of defence. The most common view of immunity has been one of a system driven by antagonistic co-evolution. Lazzaro (2008) reflects this, stating 'Natural selection may act strongly on immune systems as hosts adapt to novel, diverse, and coevolving pathogens'. Although this view is of course fair, and indeed this chapter would argue that parasitic symbionts with extracellular phases present some strong interacting partners that may comprise part of this process, a complementary view is that the evolution of these systems may be driven in part by the need to accommodate partners as much as from antagonistic interactions with parasites.
This thesis is made from the knowledge that these bacteria are common and strong interactors with insects, and that the bacteria that are present in these roles alter over time and between species. This creates the evolutionary scenario in which they can drive the evolution of these systems on a continuous basis. One can imagine the loss of an AMP being selected for by presence of a beneficial symbiont which is sensitive to it. Any subsequent loss of the symbiont (as natural enemy pressure changes) would produce selection for a replacement. Likewise, receptors that promote phagocytosis of beneficial bacteria may be lost, and replaced with other elements with a different spectrum of sensitivity.
One prediction of the thesis that immune systems evolve to accommodate the presence of beneficial symbionts is that a history of interaction with beneficial symbionts will alter sensitivity to pathogens. It is notable that many secondary symbionts occur within the gamma proteobacteria, and are closely allied to pathogens. How does any host accommodation or bacterial action that accompanies possession of a Pseudomonas strain by Pederea beetles affect susceptibility to related pathogens, and, likewise, S. symbiotica for aphids?
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