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Understanding how insect immunity is regulated requires studying the interactions of all those aspects of physiology that impact immunity. This includes both resistance and tolerance aspects of defence as well as all of the other assorted physiological systems of the insect that alter the immune response. It is hypothesized that an insect's innate immune responses is in the centre of a physiological net and the immune response is sensitive to changes throughout this net. This chapter tries to tie all of these physiological strands together and demonstrate how innate immunity alters the gross physiology of an insect and how the gross physiology, in turn, alters the immune response. An emergent property that falls out of this analysis is the prediction of several types of physiological collapse — these collapses result from positive-feedback loops that lead to amplified and damage-inducing immune/physiological responses.

This chapter investigates the different definitions of immunology, in particular the dominant definition stating that immunology is the discipline that studies the defense of organisms against pathogens. The different steps towards the autonomy of immunology as a discipline are examined, from immunization to the elaboration of a theory of immunity, and eventually the institutionalization of the domain. I propose my own definition of immunology as the discipline that studies specific interactions between immune receptors and antigenic patterns, triggering mechanisms that destroy or prevent the destruction of target antigens. I show that, contrary to what has long been believed, every organism has an immune system. I describe several examples of immune systems (in mammals, insects, plants, and even unicellulars). I close this chapter by an analysis of the concepts generally considered as central in immunology, those of “self” and “nonself.”

Hosts can avoid infections by behavioural changes and by body walls. After infection, hosts can change their behaviours to reduce the effects of parasitism. Immune defences have different arms (humoral or cellular), and organization (innate, adaptive). Innate immunity consists of a collection of different systems that are evolutionarily very old. Adaptive immunity, based on expansion of specific lymphocytes, evolved in the higher vertebrates. Immune defences are regulated tightly and based on receptors that can recognize parasites (or their activity). This triggers a complex signalling cascade that results in the production of further signalling compounds and effectors. Important protein families, e.g. the immunoglobulins, form the molecular backbone. A key to efficient defences is the diversification of receptors, such as the highly evolved somatic diversification processes of advanced adaptive immunity. The microbiota adds to defences in many ways. Immune memory and priming occur throughout the tree of life.

Sleep is a fundamental requirement for living individuals. Emerging evidence suggests that disturbances in sleep and sleep disorders play a role in the morbidity of chronic conditions including obesity and hypertension. This chapter discusses the possibility that the relationship between sleep and CVD may be mediated by inflammatory mechanisms. It examines possible effects of age, gender, ethnicity, etc., on the relationship between sleep and disease progression, along with the role of inflammation in the relationship between known sleep disorders and cardiovascular risk. In particular, the role of inflammatory activation in individuals with obstructive sleep apnoea (OSA) is examined. Whilst evidence may suggest that sleep-curtailment may lead to an increase in the inflammatory processes underlying these diseases, further research is required to determine if biologically restorative sleep can reverse or halt such disease progression.

Echinoderms are basal deuterostomes and the sister phylum to the chordates. All are marine animals with effective and robust innate immunity. Echinoderms are host to diseases in both larvae and adults, which include bald sea urchin disease, sea star wasting disease, among others that are defined by a range of different and often overlapping symptoms The diseases infect either individual animals or entire populations depending on the virulence and rate of spread and can lead to death in individuals or to mass die-offs. Pathogens include marine bacteria, typically Gammaproteobacteria and members of the Vibrio splendidus clade, as well as protists and viruses. Identify the initiating pathogen has been challenging but DNA sequencing approaches provide an avenue for pathogen identification, for differentiating between an initiating pathogen and organisms that cause the secondary infections, and for characterising changes to the normal microbiome of an infected echinoderm. Echinoderm pathologies have direct impacts on marine ecology and on aquaculture for edible species that, in some cases, can be alleviated by optimising the habitat conditions for healthy echinoderm populations.

The opportunity for arms-race evolution between host and pathogens is one reason why genes involved in immune functions are often rapidly evolving. Innate immune systems lack the degree of pathogen specificity that makes such arms races easy to initiate, but nevertheless they too harbour rapidly evolving genes. While core signalling genes retain one-to-one orthology, both recognition and antimicrobial peptide genes display rapid changes in copy number. With respect to turnover of amino acids in the proteins themselves, receptors that are involved in phagocytosis evolve the fastest, with signalling proteins also evolving rapidly as a consequence of microbial attack. Antimicrobial peptides have a comparatively slow rate of amino acid replacement. Finally, several proteins involved in viral and transposon defence are exceptionally rapid in their evolutionary rates, possibly as a consequence of an arms race process whose rate is driven by the high mutation rate of viruses.

The chapter describes the central functioning of the immune system, making clear how the substantial threat from microorganisms needs to be handled through a multitude of mechanisms. The basic principles of innate and acquired immunity are explained in everyday language from a functional perspective, as well as the for this book central process of inflammation. Striking similarities between the immune system and the central nervous system are pointed out, providing a basis for understanding interactions between the immune system on the one hand and the brain and behavior on the other. In the perspective of how the immune system and the brain can regulate each other’s activity, some “truths” in the relation between stress, sleep, and health are scrutinized.

Sjögren’s disease is an autoimmune disorder in which environmental, genetic, and hormonal factors result in the disruption of the body’s innate and acquired immune systems. The activation of interferon, the presence of autoantibodies such as anti-SSA and anti-SSB, and dietary factors promote the release of inflammatory factors; this in turn produces the release of immune complexes that, when deposited in the patient’s tissue, lead to damage. Most of the damage produced by Sjögren’s disease reflects glandular disease, but approximately 10% of patients with Sjögren’s have extraglandular manifestations of the disease. Future interventions are expected to address defects in these pathways.

After many years with little forward movement in Sjögren’s, promising approaches to disease management are on the horizon, including biomarker discoveries, new metrics to assess disease activity, and advanced imaging technologies. Some of the areas being explored are the microbiome, the role of innate immunity and the interferon pathway (with the imminent approval of anti-interferon agents), checkpoint inhibitors, new T- and B-cell therapies, as well as small interfering RNA modulators. Therapeutic targets that affect the B-cell activating factor (BAFF) are being studied by oral medicine experts along with gene therapies. Further insights elucidating what damages the ocular surface, especially from a peripheral nerve terminal standpoint, will have translational consequences. The Sjögren’s Foundation Clinical Trials Consortium has been working with pharmaceutical and biotechnology companies to make the disease a major focus in clinical investigation.

Chelicerates represent one of the oldest and second most speciose groups within the Phylum Arthropoda. Often referred to as ‘living fossils’, extant chelicerates inhabit terrestrial and aquatic ecosystems. Spiders, scorpions, ticks, and mites are usually mistaken for insects, just as horseshoe crabs are misidentified as crustaceans. The biological and commercial importance of chelicerates cannot be overstated; members represent vectors of devastating animal and plant diseases (acarids), wielders of poisons and venoms (arachnids), and critical for the detection of bacterial contaminants in pharmaceuticals (horseshoe crabs). For many of the chelicerates (e.g. pycnogonids), there is a knowledge deficit with respect to host-pathogen antibiosis and histopathological condition. From the available literature, the book lungs and book gills are critical sites of pathogen dissemination throughout the haemocoel. Recent data gathered using high throughput sequencing reveals spiders as rich sources of endosymbionts and pathobionts. More broadly, research efforts are focussed on integrated pest management strategies using acaropathogenic and araneogenous fungi for controlling terrestrial chelicerate pests. This chapter represents the first extensive review of the diseases and pathobiology of chelicerates in the context of their innate immune defences. Much information has been accrued from captive settings, such as scorpions from zoological collections and horseshoe crabs in aquaria.