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An Evolutionary Perspective on the Mechanisms of Immunosenescence

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An Evolutionary Perspective on the Mechanisms of Immunosenescence Review Immune senescence special issue. Free access sponsored by the National Institutes of Health An evolutionary perspective on the mechanisms of immunosenescence Daryl P. Shanley1, Danielle Aw2, Nancy R. Manley3 and Donald B. Palmer2 1 Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne NE4 5PL, UK 2 Infection & Immunity and Genes & Development Group, Department of Veterinary Basic Sciences, The Royal Veterinary College, London NW1 0TU, UK 3 Department of Genetics, Paul D Coverdell Center, University of Georgia, Athens GA 30602, USA There is an accumulating body of evidence that a decline age [6] (also see the article by Kovacs et al. and Panda et al. in immune function with age is common to most if not all in this issue). The adaptive immune system with high vertebrates. For instance, age-associated thymic involu- specificity to antigens first appeared some 350 million tion seems to occur in all species that possess a thymus, years ago in jawed fish, and its value is demonstrated by indicating that this process is evolutionary ancient and the fact that it has been retained, albeit with a variety of conserved. The precise mechanisms regulating immu- modifications, by all vertebrates. However, there are clear nosenescence remain to be resolved, but much of what problems as evidenced by the age-related decline in effec- we do know is consistent with modern evolutionary tiveness of vaccination [7] due to a reduction in antigenic theory. In this review, we assess our current knowledge receptor diversity [8] and impaired proliferative response from an evolutionary perspective on the occurrence of (also see the article by Chen et al. in this issue). immunosenescence, we show that life history trade-offs Following Weismann, Fisher and Haldane, the modern play a key role and we highlight the possible advantages evolutionary theory of aging has now converged on a of the age-related decline in thymic function. recognition that the strength of selection declines with age as fewer and fewer individuals remain alive. This Introduction: immunity and ageing concept was summarized by Medawar in the 1950 s [9] Potential pathogens—viral, bacterial, fungal, macropara- and more recently in terms of a ‘selection shadow’ at older site and dysfunctional host cells—present a major threat to ages [10]. The result is that mutations in late-acting genes survival, and the innate and adaptive immune systems are not effectively purged [9], such that genes with early have evolved a series of defence networks to protect the life beneficial effects but that exhibit detrimental effects in individual from such harmful agents. These systems are later life might be actively selected (i.e. antagonistic pleio- not without fault, however, and with increasing age, pro- tropy) [11]. Thus, from the point of view of physiological blems arise in functional activity. There is clear evidence of investments, reproduction at younger ages takes priority an age-related decline in effectiveness of the immune over long-term maintenance [12]. Laboratory experimen- systems of vertebrates and some invertebrates, which tation (e.g. studies in Drosophila [13–15]), observation and renders older individuals more vulnerable to infection manipulation in the field (e.g. within [16,17] and between [1,2] (also see other articles in this special issue). Moreover, species [18]), and mathematical modelling [12,19–24] have there is evidence that a compromised immune system largely supported this view [10]. The relative role of renders individuals more susceptible to other sources of mutation accumulation, antagonistic pleiotropy or physio- mortality (so-called comorbidities) [3,4]. Infectious disease logical trade-offs in governing aging is by no means has been eradicated in the developed world, and humans resolved. In general, rates of aging have an inverse are living much longer than they have commonly lived in relationship with levels of environmental mortality, which the past, which exposes the weaknesses and age-related might be modified by other factors such as age-related decline in the immune system to their full extent, making increases in size or fertility [25], population density [4] immunosenescence an important public health concern. and transfer of resources between generations [24]. The more evolutionary ancient innate system, common The immune system is active across the lifespan and is to invertebrates and vertebrates, has at its core, phagocytic frequently considered an integral part of general mainten- cells that generate reactive oxygen and nitrogen species to ance processes within the framework of life history theory damage and kill pathogens [5]. This system is fast-acting (Box 1), which provides the conceptual base for this article. and effective but is nonspecific and might cause secondary Fielding an immune defence has high physiological costs, damage to the host with long-term consequences requiring and differences exist between and within species. As a organisms to optimise their response. A further problem is system, there are clearly pleiotropic effects whereby early that phagocytic cells become functionally impaired with life survival benefits of protection against infection might present late life problems of accumulated damage Corresponding authors: Shanley, D.P. ([email protected]); (e.g. chronic inflammation or autoimmunity), sometimes Palmer, D.B. ([email protected]). referred to as inflamm-ageing (Box 1). Furthermore, there 374 1471-4906/$ – see front matter ß 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.it.2009.05.001 Available online 21 June 2009 Review Trends in Immunology Vol.30 No.7 Box 1. Key evolutionary aspects of aging Drosophila show a proinflammatory status with increasing age [27] and have a reduced capacity to produce antimicro- Life history theory This theory provides an analytical framework to describe the life bial peptides in response to infections [28], although, inter- cycle of organisms in terms of traits such as age and size at estingly, they are reported to have a higher titre with age maturity, age-specific fertility and mortality. The fundamental due to the additional inability to clear infection. The eusocial concept is that investment of resources in physiologic functions insects present a particular opportunity to examine pheno- such as growth, maintenance and reproduction determine the value of traits, and traits are optimised under resource limiting conditions types that can differ in organisms but which are genetically to maximise Darwinian fitness. highly related. In honey bees, there is clear evidence of an increased investment in the immune system as demon- Disposable soma theory strated by juvenile hormone and vitellogenin, which con- Investment in maintenance and immune function competes with reproduction for limited resources. The outcome is that systems are tributes to the enhanced longevity of hive bees relative to the not fully effective, and levels of unrepaired damage accumulate, short-lived foragers [29]. Similar patterns of immunosenes- leading to irreversible decline in organism function with age [12]. cence can also be observed in vertebrates. For instance, there is a substantial body of evidence reporting immuno- Inflamm-aging An inflammatory response is essential for survival in infectious senescence in wild populations of birds [30,31]. All studies environments, but as more people live longer lives, diseases report a decline in T-cell function, and some of B-cell func- associated with low-grade chronic inflammation such as cardiovas- tion and the innate system. A potential explanation for these cular disease, diabetes and dementias are increasing. The successful differences might be due to longevity of the study bird aged (i.e. the oldest elderly) have well-balanced pro- and anti- species [31]. The features of immunosenescence including inflammatory profiles at the level of the phenotype and genotype [91]. changes in cellular phenotype, cellular senescence and Cohort morbidity phenotype inflamm-ageing that have been identified in humans and Early life exposure to infectious disease causes damage that persists rodents have also been reported in other mammals, in- to later life. A period of decline in risk results in immediate reduction in damage with a delayed cohort effect on longevity. A striking cluding cats, dogs and horses [32–35]. For instance, in prediction is that extensions in longevity are unlikely to continue at horses, a decreased proliferative response of T cells and the same rate in the developed world [95]. telomere shortening in peripheral blood mononuclear cells have been observed in older animals [35]. Th1: Th2 ratio A Th1 proinflammatory response gives the host an advantage of Ecological immunology considers human evolution as surviving in an infectious environment; however, females are prone divided into three epidemiologic transitions. Up to around to a higher risk of spontaneous abortion. By contrast, a Th2-type 10 000 years ago, humans lived as hunter-gatherers in response is generally anti-inflammatory in nature. The balancing small and dispersed groups where the main threat was selection due to a trade-off in survival and reproduction explains persistent pathogens such as tuberculosis, herpes and persistence of apparently negative polymorphisms [107]. helminths. The main cost of a helminth infection is a Age-associated thymic involution loss of nutrition due to induced diarrhoea and vomiting. One of the hallmarks of the ageing immune system that all Interestingly,
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