Echinococcus multilocularis: parasite-specific humoral and cellular immune response subsets in mouse strains susceptible (AKR, C57BI/6J) or ‘resistant’ (C57B1/10) to secondary alveolar echinococcosis

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Abstract
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 30p.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 90p.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 ceils 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 antl‐Em2 antibodies of the IgG2a isotype were detected. Anti‐Em2 antibodies of the IgG3/lgG1 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.

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