The separation of Taenia saginata oncospheres from fecal debris.

by a single, autosomal, non-H2-linked gene and may be associated with the generation of a specific or nonspecific suppressor T cell population (Howard et al., 1981, J. Exp. Med. 153: 557568; Scott and Farrell, 1981, J. Immunol. 127: 2395-2400). Evidence that resistance to L. donovani as well as to other intracellular pathogens may be controlled by the same locus on chromosome 1 has been presented (Skamene et al., 1982, Nature 297: 506-509; Plant et al., 1982, Nature 297: 510-511). The immunologic basis for increased susceptibility of the MRL/lpr strain to L. tropica is unknown. Beginning at about 8 wk of age, animals with the lpr mutation develop progressive lymph node enlargement, T cell proliferation, and B cell hyperactivity (Pisetsky et al., 1980, J. Exp. Med. 152:1302-1310; Creighton et al., 1979, J. Immunol. 123: 2627-2636). A number of autoantibodies are produced and there is reported evidence of multiple and profound immunoregulatory disturbances (Pereira and Creighton, 1980, Clin. Immunol. and Immunopath. 15: 258-267; Dauphinee et al., 1981, J. Immunol. 127: 24832487). The lpr gene does not map to the centromere end of chromosome 17 and thus is not directly associated with the immune major histocompatibility locus; its relationship to other non-H2 loci (Bradley et al., 1979, Clin. Exp. Immunol. 37: 7-14) that influence susceptibility to L. donovani has not been investigated. Whether lprgene-mediated susceptibility to L. tropica and T. cruzi is the result of similar immunoregulatory defects is also unknown.