The effects of maternal antibodies can extend beyond the neonatal phase, shaping immune function into adulthood. integral to immune phenotypes. Furthermore, ecoimmunological studies have shown that heterogeneity in immunity at the individual and species levels can have important consequences for disease dynamics within populations and communities as well as population cycling. Herein we discuss these key research areas in ecoimmunology as they relate to three central themes: (1) immunity in the context of the whole organism, (2) heterogeneity in immunity, and (3) the broad consequences of individual variation in immunity. We conclude by reviewing future directions for ecoimmunology, focusing on those that could have important implications for public health, conservation, and wildlife management. genotypes can resist the wasps attack by producing hemocytes (blood cells) that encapsulate the eggs, destroying them (Poirie et al. 2000; Kraaijeveld et al. 2001). However, this and other defenses have costs: more resistant genotypes (i.e., those that can better control infections) also have slower feeding rates than more susceptible against the parasitoid wasps vary geographically, indicating that variable selection pressures across environments lead to local optima for immunity (Kraaijeveld and Godfray 1999). For example, humidity influences the biological pathways enabling resistance to parasitoids and, thus, can alter the costs of immunity. As a result, humidity could shape the local evolution of defenses. The Costs of Immunity Cause Trade-Offs Within Individuals The aforementioned evolutionary costs of immunity have physiological bases. For instance, the development, activation, and even mitigation of parasite defenses can impose substantial costs on organisms (Lochmiller and Deerenberg 2000). Experimental activation of immune responses can cause increases in metabolic rate and body mass loss, indicating that immunity has energetic costs (Demas et al. 2011; Ots et al. 2001; Freitak et al. 2003; Martin et al. 2003; Eraud et al. 2005; Amat et al. 2007). Nutrient availability is also critical. For example, carotenoid availability limits the expression of immune traits in juvenile (Saino et al. 2003; Klasing et al. 2006; Tyndale et al. 2008) and adult (Blount et al. 2003; Amar et al. 2004) birds and fish. Similarly, the amino acid lysine is integral to leukocyte function and the biosynthesis of proteins associated with innate immunity (Iseri and Klasing 2014). Indeed, in chickens, the lysine required during the acute-phase response to a bacterial infection is equivalent to that in 355 feathers or 17% of an egg (Iseri and Klasing 2014). Because any resources allocated to immunity are unavailable for other activities, the resource costs of immunity can drive allocation trade-offs (Norris and Evans 2000; Lochmiller and Deerenberg 2000; Ardia et al. 2011; Downs et al. 2014). For example, energy limitation underlies a trade-off between wound healing and reproduction in the ornate tree lizard (spp. and (Lazzaro et al. 2004). Furthermore, immune phenotypes are also influenced by the environment and gene-by-environment interactions. For example, resistance to the ectoparasitic mite, varies with density and temperature, resulting in an environment-dependent evolutionary trade-off. Developmental Environment and Immune Heterogeneity Early developmental experiences can also affect the expression of immune traits, sometimes Pilsicainide HCl throughout life. For example, parents can transmit antibodies to their offspring that shape immunity both immediately and in the long term (Hasselquist and Nilsson 2009). In mammals, some antibody isotypes pass across the placenta and via lactation shortly Pilsicainide HCl after birth (Grindstaff et al. 2003; Boulinier and Staszewski 2008). Maternal antibodies can also be transferred to offspring in the egg yolks of birds, fish, and reptiles (Grindstaff et al. 2003; Boulinier and Staszewski 2008). Neonates tend to be particularly vulnerable to parasites in early life. Short-term bolstering of resistance by maternal antibodies can enhance offspring growth rates and maturation (Hasselquist and Nilsson 2009). The effects of maternal antibodies can extend beyond the neonatal phase, shaping immune function into adulthood. In laboratory animals, exposure to antibodies during development altered the immune response to antigens later in life (Wikler et al. 1980; Elliott and Kearney 1992; Lundin et al. 1999). In one study of Wistar Furth rats, the effects of neonatal antibody exposure increased the immune response to a bacterial antigen in the next generation (Lundin et al. 1999). Other components of the developmental environment Pilsicainide HCl , such as food availability and parental care, can also influence immune phenotype. In Gambian villages supported by subsistence farming, adult body condition and the mass of newborns were tightly linked to the growing season; body condition was Pilsicainide HCl significantly lower during the seasonal postharvest period when little food is Pilsicainide HCl ZPK available (Moore et al. 1999). People born during the postharvest period were at higher risk of death from infectious disease, suggesting long-term impacts of early-life food limitation. Other types of parental care can.