Echinococcus multilocularis: parasite-specific humoral and cellular immune response subsets in mouse strains susceptible (AKR, C57B1/6J) or 'resistant' (C57B1/10) to secondary alveolar echinococcosis.
Parasite-specific humoral and cell-mediated immune responses were investigated in highly susceptible (AKR and C57B1/6J) and relatively resistant (C57B1/10) mice undergoing secondary alveolar echinococcosis (infection with Echinococcus multilocularis metacestode). The parasite-specific proliferative immune response of lymph node cells upon in vitro antigen stimulation remained weak in all three mouse strains. By day 30 p.i., CD4+ lymphoblast cells dominated the total population of blast cells in all three mouse strains. There was, however, an unexpectedly high proportion of CD8+ blast cells; by day 90 p.i., a marked proportional increase in CD8+ cells was seen in susceptible (AKR and C57B1/6J), but not in resistant (C57B1/10) mice. Susceptible, but not resistant mice exhibited a significantly decreased responsiveness of lymph node cells to concanavalin A (Con A) stimulation on day 90 p.i. Analysis of the humoral immune response by ELISA showed that resistance in C57B1/10 mice was associated with the ability of the host to synthesize antibodies to Em2 of the IgG3 and IgG1 isotype. Em2 is a lectin-binding carbohydrate antigen of the laminated layer. In susceptible AKR and C57B1/6J mice, low levels of anti-Em2 antibodies of the IgG2a isotype were detected. Anti-Em2 antibodies of the IgG3/IgG1 isotype, however, were absent. Differences in subclass-specific IgG responses were confirmed by immunoblot analyses. Our findings suggest that differences in antigen recognition (with respect to subsets of humoral and cellular immune components), probably controlled by non-H-2 gene(s), coupled to immune suppression modulated by CD8+ cells and/or respective cytokines, may determine susceptibility or resistance in experimental infection with E. multilocularis.
Gottstein
B
B
Institute of Parasitology, University of Berne, Switzerland.
Wunderlin
E
E
Tanner
I
I
D000818:Animals; D000909:Antibodies, Helminth / Q000096:biosynthesis*; D000917:Antibody Formation; D000947:Antigens, Helminth / Q000032:analysis; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D016827:CD8 Antigens / Q000032:analysis; D004443:Echinococcosis / Q000150:complications / Q000276:immunology*; D004445:Echinococcosis, Pulmonary / Q000209:etiology / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D006183:H-2 Antigens / Q000235:genetics; D007111:Immunity, Cellular; D007113:Immunity, Innate / Q000235:genetics; D007074:Immunoglobulin G / Q000032:analysis; D007132:Immunoglobulin Isotypes / Q000032:analysis; D008198:Lymph Nodes / Q000166:cytology / Q000276:immunology; D008214:Lymphocytes / Q000276:immunology; D051379:Mice; D008806:Mice, Inbred AKR; D008810:Mice, Inbred C57BL; D016176:T-Lymphocyte Subsets / Q000276:immunology
D000909:Antibodies, Helminth; D000947:Antigens, Helminth; D016827:CD8 Antigens; D006183:H-2 Antigens; D007074:Immunoglobulin G; D007132:Immunoglobulin Isotypes