[Regulation of defence and allergic reaction in infections with parasites].
Cytokines regulate development, differentiation and expression of effector function of the immune system. The profile of immune reactions depends on cytokine contents at the recognition of parasite. However, parasites themselves can modify immunological events and favourite these, which allow them to survive. The host immune defence can be transformed into the chronic reaction. Inflammatory reactions result from the recruitment of different cells, to the site where worms are localised. The eosinophil and mast cell migration preferentially is induced. These cells play also a major role in immediate allergic responses. Mast cells can bind allergen-specific IgE to their FcepsilonRI, the high affinity receptor for IgE. Eosinophils, through their receptors for IgG1, IgG2, IgA and IgE are mainly involved in the cytotoxic reaction directed against parasites. Crosslinking of these receptors by antigen binding will lead to subsequent release of stored mediators and cytokines. Granular materials released from mast cell accelerate inflammatory reaction and in the case of intestinal worm parasites may be involved in the expulsion phenomenon. However these cells may also induce Th2 related immunological response because they produce and release of IL-4. Eosinophils are required into the tissue and release cytotoxic and stress proteins including reactive oxygen species. Parasites are destroyed but accelerated reaction results in the destruction of host proteins and cells. Antibodies, cytokines, chemokines and adhesion molecules are essential for elevation of defence against parasites. The role of cytokines, emphasizing IL-5, and function of eosinophils, mast cells and IgE are discussed in terms of induction and effector mechanisms during parasite infections.
Doligalska
M
M
Zakład Parazytologii Instytutu Zoologii, Uniwersytet Warszawski. mdolig@eco1.biol.uw.edu.pl
D000485:Allergens / Q000276:immunology; D000818:Animals; D006790:Host-Parasite Interactions / Q000502:physiology; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology*; D007073:Immunoglobulin E / Q000096:biosynthesis; D007249:Inflammation / Q000276:immunology / Q000378:metabolism; D018836:Inflammation Mediators / Q000276:immunology / Q000378:metabolism; D010271:Parasites / Q000502:physiology*; D010272:Parasitic Diseases / Q000276:immunology*
D000485:Allergens; D018836:Inflammation Mediators; D007073:Immunoglobulin E