Abstract

Immunity is an essential function for host homeostasis through its action on the control of pathogenic organisms and malignant cells. Immune defenses also require a finely-tuned regulation to avoid collateral damage due to overreacting responses and self-attack. Because of its central role for organismal fitness, the expression of immune traits has been proposed to mediate the negative covariation (trade-offs) between life history traits. These trade-offs can involve traits that are expressed at the same age or at different ages (early vs. late life traits). The magnitude of the trade-offs (as well as the sign of the covariation between early and late life traits) has a strong environmental modulation. Early environmental conditions experienced during key stages of the development of the organism have the potential to induce long-term carry-over effects on the whole suite of life history traits, defense strategies against pathogens and longevity, through immune-mediated mechanisms. Here, we provide an overview of the possible environmental features experienced in early life that can affect defense strategies and disease at late age. Our review stresses the complexity of the synergetic effects linking environmental traits, the activation and education of the immune system, defense strategies, the expression of age-dependent life history traits, susceptibilities to infection, and immunopathology. At the current stage of knowledge, context-dependent effects seem ubiquitous, preventing to have general and consistent predictions on how the n-dimensional environment will affect pattern of disease at late age, through early-immune modulation. Perhaps due to our “simpler” environment and a better knowledge of the functioning of the immune system and its regulation, studies on humans have more consistently showed that early exposure to some environmental traits (e.g., low diversity of environmental microorganisms) is indeed associated with dysregulated immune functions and increased susceptibility to infection and inflammatory diseases at late age.

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