Immune response, diversity

For much of its life cycle a parasite s environment is its host. A principal, and potentially lethal, feature of this environment is the host immune response. Diversity in parasites interactions with this aspect of their environment may therefore be expected. The host immune response varies between different hosts and so, if this is considered as a selection pressure, it may produce the ideal conditions for the generation of diversity in immune-mediated parasite-host interactions. 

In 1971, levamisole, an anthelmintic compound widely used in catde and swine, was shown to improve the effects of an experimental Brucella abortus vaccine in mice. Since that time, the veterinarians and physicians have explored the effects of levamisole in such diverse areas as arthritis, lupus erythematosis, cancer therapy, respiratory diseases, Newcastle disease, foot-and-mouth disease, mastitis, and vaccine potentiation. Although the exact mechanism of action has as yet not been deterrnined there is substantial evidence that, under defined circumstances, levamisole can augment the animal s natural immune response (9). New immunostimulants include Staph Ijysate acemannon, NLAB-31. 

Other contributions to this book have taken a molecular view of parasitic nematodes, yet molecules make only a rather brief appearance here. This chapter has tried to show that parasitic nematodes are fascinatingly and tantalizingly diverse at a phenotypic level. It has focused particularly on diversity in phenotypes that are apparent in response to environmental conditions within or outside a host. The interaction of parasites with within-host factors is a major current research effort. However, helminth immunology is particularly notable for its inattention to diversity, especially when compared with the immunology of parasitic protozoa (Read and Viney, 1996). Observations of the interaction of host immunity with subsequent development in S. ratti show the potential power of such interactions. It is also clear that a principal mechanism of the action of host immune responses is against nematode fecundity (Stear et al., 1997). This is likely to be a molecularly complex interaction. Understanding this interaction, as well as variation in the interaction is interesting, but could also form the basis of control by transmission-reduction rather than eradication per se. 

Since the identification of PAF in the early 1970 s, the autacoid has steadily emerged as a crucial mediator of diverse pathologies. Indeed, PAF is a potent mediator of anaphylaxis and inflammation and is also implicated in shock, graft rejection, renal disease, ovoimplantation and certain disorders of the central nervous system (CNS) [36,44]. There is also accumulating evidence that PAF is capable of modulating the immune response [45, 46]. 

Unnatural amino acids can possess such diverse structures that there are a number of them that may be used for purposes previously unidentified. For instance, nitrophenylalanine (16), originally used as a distance probe to quench the fluorescence of tryptophan, has recently been found to stimulate potent immune responses for novel immunogenic applications. 

The synthetic analogs of cortisol are useful in the treatment of a diverse group of diseases unrelated to any known disturbance of adrenal function (Table 39-2). The usefulness of corticosteroids in these disorders is a function of their ability to suppress inflammatory and immune responses and to alter leukocyte function, as previously described and as described in Chapter 55. These agents are useful in disorders in which host response is the cause of the major manifestations of the disease. In instances in which the inflammatory or immune response is important in controlling the pathologic process, therapy with corticosteroids may be dangerous but justified to prevent irreparable damage from an inflammatory response—if used in conjunction with specific therapy for the disease process. 

Fibrosis resulting in the loss of normal organ structures is the hallmark of chronic rejection. The fibrosis may be due to wound healing, which is then followed by the cellular necrosis of acute rejection. However, it must be pointed out that chronic rejection develops many times in the absence of acute rejection. Fibrosis may be a result of several diverse factors such as equation of chronic rejection with chronic delayed-type hypersensitivity reaction, injury to blood vessels and resulting response to chronic ischemia, the proliferation of smooth muscle cells in the intima of arterial walls producing vascular occlusion, or persistent viral infections that will induce cellular immune response. 

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