Summary Reptiles are ectothermic amniotes, providing the key link between ectothermic anamniotic fishes and amphibians, and endothermic amniotic birds and mammals. A greater understanding of reptilian immunity will provide important insights into the evolutionary history of vertebrate immunity as well as the growing field of eco-immunology. Like mammals, reptile immunity is complex and involves innate, cell-mediated and humoral compartments but, overall, there is considerably less known about immune function in reptiles. We review the current literature on each branch of the reptilian immune system, placing this information in context to other vertebrates. Further, we identify key areas that are prime for research as well as areas that are lagging because of lack of reagents in non-model systems.

Neuropathic pain refers to a variety of chronic pain conditions with differing underlying pathophysiologic mechanisms and origins. Recent studies indicate a communication between the immune system and the nervous system. A common underlying mechanism of neuropathic pain is the presence of inflammation at the site of the damaged or affected nerve(s). This inflammatory response initiates a cascade of events resulting in the concentration and activation of innate immune cells at the site of tissue injury. The release of immunoactive substances such as cytokines, neurotrophic factors, and chemokines initiate local actions and can result in a more generalized immune response. The resultant neuroinflammatory environment can cause activation of glial cells located in the spinal cord and the brain, which appear to play a prominent role in nociception. Glial cells, also known as neuroglia, are nonconducting cells that modulate neurotransmission at the synaptic level. Glial cells can be subdivided into two primary categories: microglia and macroglia, which include astrocytes and oligodendrocytes. Astrocytes and microglia are known to play a role in the development, spread, and potentiation of neuropathic pain. Following peripheral nociceptive activation via nerve injury, microglia become activated and release pro-inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6, thereby initiating the pain process. Microglia propagate the neuroinflammation by recruiting other microglia and eventually activating nearby astrocytes, which prolongs the inflammatory state and leads to a chronic neuropathic pain condition. Our review focuses on the role of glia and the immune system in the development and maintenance of neuropathic pain.

Measures of body condition, immune function, and hematological health are widely used in ecological studies of vertebrate populations, predicated on the assumption that these traits are linked to fitness. However, compelling evidence that these traits actually predict long-term survival and reproductive success among individuals in the wild is lacking. Here, we show that body condition (i.e., size-adjusted body mass) and cutaneous immune responsiveness to phytohaemagglutinin (PHA) injection among neonates positively predict recruitment and subsequent longevity in a wild, migratory population of house wrens (Troglodytes aedon). However, neonates with intermediate hematocrit had the highest recruitment and longevity. Neonates with the highest PHA responsiveness and intermediate hematocrit prior to independence eventually produced the most offspring during their lifetime breeding on the study site. Importantly, the effects of PHA responsiveness and hematocrit were revealed while controlling for variation in body condition, sex, and environmental variation. Thus, our data demonstrate that body condition, cutaneous immune responsiveness, and hematocrit as a neonate are associated with individual fitness. Although hematocrit's effect is more complex than traditionally thought, our results suggest a previously underappreciated role for this trait in influencing survival in the wild.

SUMMARYThe primary function of the immune system is to protect the organism from invading pathogens. In vertebrates, this has resulted in a multifaceted system comprised of both innate and adaptive components. The immune system of all jawed vertebrates is complex, but unlike the endothermic vertebrates, relatively little is known about the functioning of the ectothermic vertebrate immune system, especially the reptilian system. Because turtles are long-lived ectotherms, factors such as temperature and age may affect their immune response, but comprehensive studies are lacking. We investigated variation in immune responses of adult male and female red-eared sliders (Trachemys scripta) across the entire active season. We characterized seasonal variation in innate, cell-mediated and humoral components via bactericidal capacity of plasma, delayed-type hypersensitivity and total immunoglobulin levels, respectively. Results indicate that all immune measures varied significantly across the active season, but each measure had a different pattern of variation. Interestingly, temperature alone does not explain the observed seasonal variation. Immune measures did not vary between males and females, but immunoglobulin levels did vary with age. This study demonstrates the highly dynamic nature of the reptilian immune system, and provides information on how biotic and abiotic factors influence the immune system of a long-lived ectotherm.

Summary1. Life history theory predicts that immunity should be plastic and reflect environmental contexts. However, individual variation in immune investment may arise not just because of individual adjustment, but because of developmental, physiological, genetic or immunological constraints which lead to non-adaptive responses by limiting or eliminating flexibility in immune investment. Constraints can arise because organisms are single integrated units with interconnected and interacting components, in which physiological and genetic control mechanisms may limit or constrain immunity. We review some of the key underlying genetic and physiological factors that may constrain the occurrence and intensity of immune responses. 2. A major part of individual variability may rest on variation in genetic background. Geneticbased constraints can limit or influence immune responses, particularly through pleiotropy and epistatic interactions. In addition, genetic variation, an important driver of variation in antigen recognition and immune system polarization, can be constrained through linkage disequilibrium and genetic drift. Epigenetic changes can also constrain or limit immune responses in future generations based on individual experience. 3. The immune system itself can influence individual flexibility in immune investment. Throughout development individuals face tradeoffs within the immune system that favour the expression of one trait at the expense of another. Ontogenetic differences can cause juveniles and adults to produce entirely different immune responses to the same pathogen. T-helper 1 (Th1) ⁄ T-helper 1 (Th2) polarization during infection also imposes constraints upon an individual's immune responsiveness, with the consequence that hosts cannot simultaneously mount strong responses using both Th1 and Th2 cells. In addition, evidence suggests that flexibility in immune responses becomes constrained with age through accumulation of memory cells at the expense of naı¨ve cells, decreased function of cells involved in adaptive and innate immunity, and programming of HPA-immune interactions. 4. In summary, selection on a particular immune trait can have effects on other immune components or phenotypic characters, as revealed by artificial selection studies. In particular selection for increased investment in compartments of the immune system leads to decreased investment in other competing life history functions and ⁄ or marked changes in other immune components. The role of past experience, even the past experience of parents, may limit and constrain immune responses through influencing the ontogeny of immunity, as well as through epigenetic influences.