Characterization of T‐cell immune responses of Echinococcus multilocularis‐infected C57BL/6J mice

Abstract

Specific and non-specific parasite-induced changes in lymphocyte responses were analysed in C57/BL/6J mice after intrahepatic infection with Echinococcus multilocularis. Spleen cells harvested at selected times after infection were in vitro stimulated with mitogens or a crude soluble parasite extract (EmAg) at an optimized dose. Cell proliferative responses to Con-A were not modified by the infection over the first 22 weeks. In contrast, LPS-induced responses were decreased from the 13th week. A strong CD4+ proliferative T-cell response to the parasitic extract of infected mouse spleen cells was observed at the early stage of infection. This response then progressively decreased but remained significantly higher than that of control mice until the 19th week of infection. Cytokine production was investigated after in vitro EmAg stimulation of spleen cells. IFN-gamma, IL-2, IL-5 were produced within the first weeks after infection whereas the detection of IL-10 was slightly delayed. Thus, the promotion of the disease does not appear associated with the expansion of one rather than another T-cell subset in C57BL/6J mice. A general immunosuppression affecting both mitogenic and parasite-specific T-cell responses was observed at the end of the infection.

Triggering and modulation of the host-parasite interplay byEchinococcus multilocularis: a review

“…E. multilocularis appears to induce skewed Th2-responses (Emery et al 1996). Based on in vitro and in vivo studies, Th2 dominated immunity was associated with increased susceptibility to disease, while Th1 cell activation through IL-12 (Emery et al 1996), IFNc (Jenne et al 1998 ;Liance et al 1998), TNFa (Amiot et al 1999 and IFNa (Godot et al 2003) was suggested to induce protective immunity in AE Vuitton, 2003). The intense periparasitic granulomatous infiltration indicates an intense host-parasite interaction, and the involvement of cellular immunity in control of the metacestode growth kinetics is strongly suggested by experiments carried out in T cell-deficient mouse strains (Dai et al 2004).…”

“…In murine infections with E. multilocularis, the involvement of cellular immunity in controlling the infection is strongly suggested by the intense granulomatous infiltration observed in the periparasitic area of lesions (Bresson-Hadni et al 1990 ;Emery et al 1996). E. multilocularis appears to induce skewed Th2-responses (Emery et al 1996).…”

Major Carbohydrate Antigen ofEchinococcus multilocularisInduces an Immunoglobulin G Response Independent of αβ+CD4+T Cells

“…Despite the public health importance of AE in areas such as Central Europe, Alaska, China, and others, knowledge of the parasite's survival strategy, parasite-host interactions, and immune control of E. multilocularis infection is still not satisfactory with respect to molecular parasite components, in contrast to the already well-explained imbalanced host immune response (2,15,17,24,30,45).…”

Current trends in tissue-affecting helminths

“…T he involvement of cellular immunity in controlling the infection is strongly suggested by the intense granulomatous infiltration observed in the periparasitic area of lesions in experimentally infected mice (Bresson-Hadni et al, 1990;Emery et al, 1996;Vuitton et al, 1989). Immunodeficient athymic nude and SCID mice as well as HIV-co-infected patients (Sailer et al, 1997;Zingg et al, 2004) exhibited high susceptibility to infection and disease, thus suggesting that the host cell mediated immune response plays an important role in suppressing the larval growth.…”

“…Immunodeficient athymic nude and SCID mice as well as HIV-co-infected patients (Sailer et al, 1997;Zingg et al, 2004) exhibited high susceptibility to infection and disease, thus suggesting that the host cell mediated immune response plays an important role in suppressing the larval growth. E. multilocularis appears to induce skewed Th2-responses (Emery et al, 1996). Based on in vitro and in vivo studies, Th2 dominated immunity was associated with increased susceptibility to disease, while Th1 cell activation through IL-12 (Emery et al, 1996), IFNγ Jenne et al, 1998), TNFα (Amiot et al, 1999) and IFNα (Godot et al, 2003) was suggested to induce protective immunity in AE Vuitton, 2003 hampered by the fact, that the parasite synthesizes a carbohydrate-rich laminated layer in order to be protected from host effector mechanisms (Gottstein & Hemphill, 1997).…”