Immunopathological mechanisms in the induction of parasitic diseases with particular reference to type III hypersensitivity reactions

Abstract

During the primary immune response to an infectious agent, specific memory cells are generated which enable the immune system to respond more rapidly and efficiently to re-exposure to the same agent. Under normal circumstances, this acquired resistance leads to the effective elimination of the agent, and recovery. However, under certain circumstances these secondary infections, rather than aiding recovery, actually produce tissue damage and often contribute to the disease process. This stage has been termed hypersensitivity and such hypersensitivity reactions play an important role in the immunopathology of several diseases. Coombs & Gell (1963) have classified hypersensitivity into four types of reaction. Types I, II and III involve antibody-mediated processes whereas type IV is mediated solely by lymphocytes. Many parasitic infections have characteristics which would appear to predispose the host to the development of hypersensitivity states and consequent immunopathology. These include (1) the chronicity of the infections, (2) the release of parasite antigens in large amounts and their persistence in the circulation and host tissues, (3) the sharing of antigens between parasite and host and (4) the ability of the parasite to damage host tissues and alter their antigenicity. However, direct evidence that these mechanisms lead to the development of immunopathology in parasitic infections is limited. In this article, these four types of hypersensitivity will be briefly discussed in the context of the immunopathology following parasite infection. There then follows a more extensive consideration of type III hypersensitivity with particular emphasis on the mechanisms underlying the development of immune-complex mediated disease.