Immunity and internal defence. In parasitoses of vertebrates cyclically transmitted by an invertebrate intermediate host or vector, the parasite has to resist two basically different defence systems, the immune apparatus in the vertebrate and the internal defence system (IDS) in the invertebrate. The reaction of the latter is often called "innate immunity". Unequivocal terminology is essential if defence reactions of vertebrate hosts have to be compared with those of invertebrates at the population level, especially with respect to their influence on the epidemiology of a cyclically transmitted parasite. The term "innate immunity", however, causes confusion and inconsistencies.
An innate immunity in the literal sense does not exist, in the same way that an innate language does not. However, an innate resistance does. Moreover, immunity cannot be equated with resistance. For example, delayed type hypersensitivity (DTH) is an immune reaction, but not a kind of resistance.
Resistance means survival in the presence of a potentially lethal pathogen and may be structurally based without specifity. Each kind of specific resistance needs recognition mechanisms and is based on the activation of an organ system by which the power of defence increases adaptively with prolonged contact. The specifity of its reactions depends on pattern recognition receptors (PRRs). Their structures are genetically determined.
Immune reactions and innate resistance reactions have an afferent and an efferent branch, i.e. mediators for recognition and reaction, respectively (Box 8.3, page 288). Both are reversible; however, innate resistance acts immediately, whereas acquired resistance or immunity acts with a reaction delay, called latency. In contrast to innate resistance, acquired immunity creates memory and, in the case of a secondary contact with the same antigen, it is activated without latency but with increased force. The secondary reaction is specific, i.e. only quantitatively different from the corresponding primary reaction. This is not true for innate resistance. Primary and secondary contact reactions are equal (see below: Box "Mechanisms of resistance").
Immune reactions involve cell cooperation via an interaction of B- and T-cells, which are highly specific to each individual. The interactions of these cells are controlled by MHC restriction. Innate resistance reactions are not controlled by cooperation between an individuals own cells. The accumulation of macrophages on a foreign surface, as observed in invertebrate reactions, cannot be regarded as such a cooperation, because it is not controlled by a mechanism like the MHC system.
The structures that react in recognition of infection/invasion in both systems are similar or even equal in vertebrates and invertebrates. Both (also plants) possess an immediately reacting system for the recognition, i.e. the discrimination of "foreign" and "own" (but not of "self" and "non-self", which is controlled by the MHC). Their cells are covered by a series of preformed chain-like receptors designed as pattern recognition receptors (PRRs). They react on contact with molecular repeating structures, e.g. on the surface of a microbial pathogen (pattern associated molecular patterns, PAMPs). This contact creates a signal cascade that leads to the elimination of the pathogen. Physically, the structures of PRRs and PAMPs are complementary. Because of this molecular complementary compatibility, the arsenal of PRRs together with the PAMPs constitute the affectory branch of the defence reaction. In order to eliminate the pathogen completely, an effectory branch is necessary, consisting of an arsenal of proteins and cells. This is differently equipped in vertebrates and invertebrates. The latter lack an acquired resistance, whereas vertebrates combine innate and acquired resistance or immunity.
Whether innate resistance can be regarded as a precursor of acquired immunity is open to debate. However, the argument should concentrate on the question "What is the basis of the memory of molecular structures?" To call innate resistance "innate immunity" is wishful thinking and obscures more than it elucidates. In vertebrate defence, the immediately reacting form of innate resistance is indispensable, otherwise an attack on an organism would lead to death before the required time span of latency that the immune reaction requires has elapsed.
Similar protein structures and their corresponding similar genetic codes do not necessarily provide reasons for assuming common evolutionary origin as is shown in the following example. Light-sensing cells contain proteins (visual purple) that change their molecular structure producing electric impulses when light quanta impinge upon them. Their effectivity increases when they are equipped with structures of refractive properties. Each of these structures are most probably similar with respect to their physical properties. The coding genes may even also be similar in both cases. Lenses are present in both invertebrates and vertebrates. Given that all light-sensitive and light-refractive proteins are composed of similar molecular structures (which is most probably true), then they are probably encoded by similar sequences in the genome. We cannot, however, conclude from this that all animal light-sensitive cells, the various constructions of their eyes and finally the innate or adapted visually controlled behaviour of these animals have a monophyletic origin.
Innate resistance acts immediately but returns to its original condition when the pathogen has disappeared; the reaction is completely reversible, genetically determined and therefore inherited but not memorized. Acquired resistance starts at the first contact of the individual with pathogen, after a period of latency but, at the second contact with the same foreign body, the reaction starts immediately and with increased power. This is an immune reaction in the strict sense and is memorized but not inherited; it fulfils the basic feature of a protective immunity.
In analogy to an arms race between predator and prey species at the trophic level, a balance of power is established between parasites and their hosts. In order not unduly to stress their own resources, parasites control their propagation by specific interactions with the host. Defence mechanisms work only at the level of the individual host. At the population level, the result is a balance between the antagonistic mechanisms controlling susceptibility and resistivity, on both features the host specifity of any parasite is based.