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
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
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DOI:
10.1111/j.1365-2249.1994.tb06549.x
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发表时间:
1994-05-01
影响因子:
4.6
通讯作者:
TANNER, I
中科院分区:
文献类型:
--
作者:
GOTTSTEIN, B;WUNDERLIN, E;TANNER, I
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.