Immunity to Parasites: How Parasitic Infections are Controlled

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This completely updated second edition provides a clear account of how immune responses operate and how parasites can evade immunity.

Parasites have evolved to exploit hosts' bodies, whereas hosts have evolved immune systems to control infections. Host-parasite interactions therefore provide fascinating examples of evolutionary "arms-races" in which the immune system plays a key role. Including an expanded section on anti-parasite vaccines, the text focuses on modern research in immunoparasitology directed at understanding and exploiting the capacity to develop effective anti-parasite immunity.

The experimental basis of this research is emphasized throughout. The text is aimed at undergraduates and postgraduates with interests in either parasitology or immunology and contains introductory sections on these topics. Read more Read less. Cambridge University Press; 2 edition August 13, Language: Be the first to review this item Amazon Best Sellers Rank: Related Video Shorts 0 Upload your video. Try the Kindle edition and experience these great reading features: Customer reviews There are no customer reviews yet.

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Get fast, free shipping with Amazon Prime. Your recently viewed items and featured recommendations. View or edit your browsing history. One of the most interesting aspects of the role of NO in malaria is as a possible cause of the coma associated with cerebral malaria. Malaria also demonstrates one of the fundamental problems in trying to control parasitic infections, getting the balance between protection and counterprotection right. The pathology associated with the granulomatous response to schistosome eggs has also had to be reinterpreted. These granulomas have long been considered to be due to a T H 1-mediated delayed-type hypersensitivity DTH response but it is now known that most of the inflammatory cells involved are eosinophils and that the development of granulomas is inhibited by the T H 1-activating cytokine IL Basophils and mast cells mediate allergic responses, where they are the central cells involved in IgE-induced immune responses to parasites and other allergens.

Both cell types are derived from BM precursors, but they have a very different ontogeny. Basophils have a single lobed nucleus and characteristic intensely staining purple granules that may cover the nucleus see Fig. These granules contain glycosaminoglycans, predominantly heparin. Basophils differentiate from BM progenitors and are released from the BM as mature cells, where they circulate briefly, with a lifespan similar to that of neutrophils. Maturation is induced in response to IL-3, which serves both to induce basophilic differentiation and to mediate activation of mature basophils.

Although IL-3 is the primary mediator of basophil development, studies of ILnull mice have demonstrated that it is not required for baseline production of basophils. It is, however, required for the induction of basophilia in response to parasitic infection. Mast cells arise from BM precursors but are released into the circulation as immature cells. They circulate only briefly in the peripheral blood before migrating to the tissues, where they complete their maturation. There remains some question about whether mast cells and basophils arise from a common precursor.

It is clear that SCF is especially effective in inducing mast cell proliferation; in fact, activating mutations in c-Kit, the SCF receptor, is the underlying molecular defect in most cases of systemic mastocytosis. Mast cells and basophils are functionally related effector cells of hematopoietic origin that are implicated in allergy, type 2 immune responses to parasites, and innate immunity.

Both release histamine and generate a variety of other inflammatory mediators in response to both IgE- and non-IgE-mediated activation.

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However, there are important differences between mast cells and basophils in terms of their developmental origins, morphology, distribution, and mechanisms and responses to stimulation. Whereas mast cells are normal residents of all vascularized tissues, basophils are recruited to mucosal sites in response to inflammation. Both cells are important effectors of hypersensitivity responses, and both play roles in host defense as well as the pathophysiology of a variety of disease processes. Unchecked mast cell growth underlies mastocytosis, a group of disorders defined by a constellation of symptoms resulting from excessive mast cell products and infiltration into tissues.

The precise and likely multiple mechanisms leading to the diverse clinical manifestations of lymphatic filariasis have not been established. However, several factors have been suggested to underlie the development of lymphedema, including parasite-derived factors that may be responsible for the lymphatic dilatation seen early in infection, host genetic susceptibility, secondary bacterial infections, specific host adaptive immune responses to parasite antigens, and inflammatory responses to dying or dead parasite material.

Establishing the relative importance of these diverse factors and a central unifying hypothesis to explain the pathogenesis of human lymphatic filariasis has been difficult because the onset of disease occurs over a period of years or decades and because of the marked heterogeneity in transmission and disease in geographically distinct filarial-endemic areas.

The immunologic basis for the relative lack of pathology seen in the majority of individuals with patent infection, however, has been reasonably well studied in both cross-sectional and longitudinal population-based studies. Studies in animal models and in vitro human systems have suggested that the initial immune response to infective stage larvae L3 and to the next developmental stages L4 and early adult stages are dominated by proinflammatory and a mixed Th1-like and Th2-like T-cell responses.

With the onset of patency when microfilariae appear in the blood , there is a marked diminution of the parasite antigen-specific T-cell responses both proliferation and Th1 cytokine responses that is primarily mediated by interleukin IL and other regulatory cell populations e. Examination of protective immunity in lymphatic filariasis in human populations has been extraordinarily difficult. However, population-based studies have identified groups of individuals who appear to be infection-free despite long-term exposure to the filarial parasites.

When looked at immunologically, on balance cells from these individuals are more likely to respond to parasite antigen than were those with patent infection. The best evidence, however, for the induction of protective immunity has come from studies in animals jirds, cats, ferrets permissive for Brugia spp. Travis, in Advances in Immunology , The main activity of the immune system is protection against infections. Immunocytes leukocytes are mainly lymphocytes and they produce humoral antibody; mainly B-cell or cell-mediated mainly T-cell responses that are central to the immune defences.

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B lymphocytes evolve into plasma cells, which produce antibodies to protect against extracellular organisms Fig. Antigens are processed by antigen-presenting cells APC and presented to T lymphocytes, which fulfil most other immune functions i. Macrophages and polymorphs are the main professional phagocytes; macrophages and macrophage-like cells are widely distributed in the lymphoreticular reticuloendothelial system Fig. More than 70 types of leukocyte are recognized and defined by their cluster of differentiation CD antigens, which in turn are recognized by monoclonal antibodies.

Immunocytes are, in large part, regulated by cytokines produced by a variety of cells. Cytokines produced by lymphocytes are termed lymphokines, and those that act between leukocytes are called interleukins see Appendix Cytokines may also induce systemic effects, such as the acute-phase response see above. The movement of leukocytes between the blood and tissues depends on leukocyte—endothelial cell adhesion molecules known as selectins, integrins and the immunoglobulin gene superfamily IgSF; intercellular adhesion molecules [ICAMs] and lymphocyte functional antigen 3 , and over 20 other proteins.

Antibody production is modulated by T lymphocytes, which either assist T-helper cells or moderate T-suppressor cells. Immunoglobulins antibodies are of different classes Table Complement and polymorphonuclear leukocytes PMNLs are essential to phagocytosis and inflammation. Cell-mediated responses are usually protective, and macrophages are also phagocytic.

Macrophages and dendritic cells intimately involved in antigen processing and the transference of information to lymphocytes are called antigen-processing cells APCs. Phagocytes PMNLs and macrophages are attracted towards antigens, via activated complement after an antigen—antibody reaction, and can ingest and often kill microbes that are opsonized i. During phagocytosis or attempted phagocytosis of, for example, immune complexes, these phagocytes may discharge degradative enzymes lysosomal enzymes , which can cause local tissue damage.

Large granular lymphocytes LGLs; or null cells are non-phagocytic cells that mediate NK cell activity and antibody-dependent cellular cytotoxicity ADCC — the binding and lysis of antibody-coated target cells.

Immunology of parasitic infections. - PubMed - NCBI

NK cells recognize malignant or foreign cells by a non-immune mechanism. Basophils and mast cells have surface receptors for IgE, and contain histamine, prostaglandins, leukotrienes and proteases. They are involved in immune responses to parasites and in the immediate type of hypersensitivity responses Ch. The enzyme cyclo-oxygenase COX produces prostaglandins and thromboxane, while the enzyme 5-lipoxygenase produces leukotrienes.

Antigens are processed by antigen-presenting cells, such as macrophages and Langerhans cells in epithelia, and presented to T cells in association with class I or II MHC molecules. T lymphocytes originate in bone marrow but differentiate within and are under the control of the thymus hence T , acquiring immunological competence there, a process that requires the normal functioning of purine metabolism. T cells all have T-cell receptors, highlighted by the CD3 surface marker. When activated by antigens, T lymphocytes produce lymphokines, which, among other activities, can modulate nearby cells, particularly macrophages, resulting in CMI type IV immune responses.

These are particularly important in the defence against some intracellular bacteria, such as mycobacteria, and against viruses and fungi, graft rejection, graft-versus-host reaction, delayed hypersensitivity and defences against cancer cells. Circulating T lymphocytes differentiate into CD4 cells — mainly helper T cells that are antigen-processing and can recognize MHC class II antigens, and can induce B-cell differentiation, induce CD8 cytotoxic T-cell proliferation, produce various soluble mediators lymphokines and regulate erythropoiesis.

CD4 helper T cells are either Th1 or Th2. Circulating T lymphocytes can also differentiate into CD8 cells, which recognize MHC class I antigens and are one type of cytotoxic or suppressor T cell; they are important in eliminating virus-infected cells.

To summarize, T-cell proliferation and differentiation are regulated by many cytokines, including interleukins, interferons, tumour necrosis factors and transforming growth factors. Cytokines generally function as local signals for cell growth, differentiation, activation, inhibition, apoptosis or chemotaxis, but may also induce systemic effects such as acute-phase responses fever, CRP, osteoclast activation, platelet release induced by IL-1, IL-6 and TNF.

There are four subclasses of IgG, and selective deficiencies of these can develop. Thus, when there is a strong suspicion of a humoral immunodeficiency based on clinical grounds but the total IgG is normal, quantitative measurement of individual subclasses is indicated. Assessment of antibody function is necessary. Antibody titres after immunization with protein antigens e. Indirect information about T-lymphocyte function may be obtained by counting peripheral blood T lymphocytes.

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