Identification of a genetic locus, Rsm-1, controlling protective immunity against Schistosoma mansoni.
Mice of most inbred strains develop moderate to high levels of resistance to challenge infection on vaccination with radiation-attenuated cercariae of Schistosoma mansoni. P strain mice, however, fail to display significant protective immunity after exposure to the same vaccine. To examine the genetic basis of this polymorphism in host immunity, vaccine-induced resistance was examined in (C57/BL6J X P/N)F1, F2, and reciprocal backcross generations. The defective immunity which characterizes the P strain parent was found to be inherited in a fully recessive manner and to be controlled by a single genetic locus, which we have designated Rsm-1. Linkage analyses revealed that Rsm-1 is not genetically associated with the major histocompatibility complex (chromosome 17), the immunoglobulin heavy chain locus (chromosome 12), or a single locus influencing defective anti-schistosomulum IgM antibody responses in the P parental stock. These data provide the first example of single gene control of vaccine-induced immunity against a helminth infection. Because P mice are also defective in their capacity to develop tumoricidal macrophages and in their immunity to Leishmania major, genes encoded by the Rsm-1 locus may play a general role in resistance to infection and malignancy.
D000818:Animals; D005802:Genes, MHC Class II; D005808:Genes, Recessive; D008040:Genetic Linkage; D007075:Immunoglobulin M / Q000276:immunology; D007153:Immunologic Deficiency Syndromes / Q000235:genetics; D008285:Major Histocompatibility Complex; D051379:Mice; D008815:Mice, Inbred Strains / Q000235:genetics / Q000276:immunology*; D012555:Schistosomiasis mansoni / Q000235:genetics / Q000276:immunology*
D007075:Immunoglobulin M