Cell-mediated damage to helminths.
Although it is difficult to draw any sweeping conclusions that would be applicable to all helminth infections, the main features that are emphasized in this review may be summarized briefly. Pathogenic helminths, although extremely diverse in structure and behaviour, have one common feature, namely that they present to the host's defenses large, non-phagocytosable surfaces. Because of this, they are susceptible to a range of effector mechanisms differing either quantitatively or qualitatively from those that are active against other parasites or against normal or abnormal host cells. As an extreme example, the various types of cytotoxic lymphocyte, with one interesting exception, are inactive against helminths. Instead, helminth infections are characterized by high IgE responses and increased numbers of circulating eosinophils. Such eosinophils are activated, and show a marked capacity to kill a variety of target helminths in vitro. Further activation may occur in response to mast cell mediators released as a result of IgE-dependent degranulation; and IgE, as well as IgG and complement, can mediate eosinophil attachment and killing. It may therefore be suggested that the eosinophil/IgE/mast cell axis represents a powerful host defense against helminth infections. IgE can also mediate macrophage-dependent killing of several helminths, a process which involves a functional change in the macrophage, resembling activation. Although eosinophil-mediated and IgE-dependent macrophage-mediated effects are particularly potent, other effector cells are not excluded: in certain circumstances, neutrophils and conventionally activated macrophages may be equally or more effective. Neutrophils appear to act solely by oxidative killing mechanisms, whereas degranulation and the release of toxic granule contents is equally or more important in eosinophil-mediated damage. Different stages of different helminths vary in their degree of susceptibility to different mechanisms. Eosinophils appear to be somewhat less active than neutrophils against ensheathed nematodes, whereas trematodes and exsheathed nematodes are highly susceptible to eosinophil attack. In many experimental helminth infections, studies in vivo suggest a role for antibody-dependent cell-mediated immune effector mechanisms. The identity of the effector cell is difficult to establish because of a lack of techniques for specific manipulation of individual cell types, but histological studies frequently point to a strong eosinophil or macrophage involvement. The development and analysis of in vitro assays allows the study of immune effector mechanisms in man.(ABSTRACT TRUNCATED AT 400 WORDS)
D000818:Animals; D002589:Cestoda / Q000276:immunology; D004195:Disease Models, Animal; D004804:Eosinophils / Q000276:immunology; D006098:Granulocytes / Q000276:immunology; D006373:Helminthiasis / Q000276:immunology; D006376:Helminths / Q000276:immunology*; D006801:Humans; D007111:Immunity, Cellular; D007158:Immunologic Techniques; D066298:In Vitro Techniques; D007814:Larva / Q000276:immunology; D008214:Lymphocytes / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D009348:Nematoda / Q000276:immunology; D051381:Rats; D014200:Trematoda / Q000276:immunology