Abstract
The parasite Trichinella spiralis has its whole life cycle in one host. Definite proof of infection resides in the demonstration of muscle larvae. The contact between the host and the parasite during the infection results in a variety of host-parasite interactions including stimulation of specific humoral and cellular immune responses. Protective immunity is developed, but as in many other parasitic infections, immune protection is not complete. It is clearly T-cell-dependent (reviewed by Wakelin, 1978), and a number of observations indicate that antibody-dependent cell cytotoxicity may be involved. It has been shown that specific circulating antibodies belong to various immunog- lobulin classes, predominantly IgG but also IgM and IgA. In man, a high level of total IgE has occasionally been demonstrated (Rosenberg et al., 1971; Ljungström, 1974; Pattersson et al., 1975; Barrett-Connor et al., 1976; Matossian et al., 1977) and, in a few cases, specific IgE antibodies (Stumpf et al., 1981). Data on specific cell-mediated immunity provoked by T. spiralis in human are very limited. A few workers (Sladki, 1960; Chicoine et al., 1966) have reported delayed-type hypersensitivity using skin tests in the diagnosis of trichinosis in epidemiological studies, but the significance of the delayed reaction is not known. In experimentally infected animals or animals immunized with T. spiralis antigen, delayed hypersensitivity including macrophage inhibition has been
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Ljungström, I. (1983). Immunodiagnosis in Man. In: Campbell, W.C. (eds) Trichinella and Trichinosis. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-3578-8_12
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