Triggering and modulation of the host-parasite interplay by<i>Echinococcus multilocularis</i>: a review

Mejri, Naceur; Hemphill, Andrew; Gottstein, Bruno

doi:10.1017/s0031182009991533

Cited by 29 publications

(30 citation statements)

References 104 publications

(128 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A similar increase of susceptibility, associated with a decrease of delayed type hypersensitivity was also observed in E. multilocularis infected mice treated with ciclosporin, which interferes in IL-2 production by Tcells (Liance et al, 1992). Principally, upon experimental infection, immunocompetent mice elicit a cell-mediated immune response, which is so far inefficient as it impairs, but does not inhibit, the proliferation of the metacestode (Dai et al, 2004;Mejri et al, 2010). It has been shown that the type of the primary immune response toward infection, initially Th1-oriented, got progressively Th2-oriented (Mejri et al, 2011a) during the progressive growth of the metacestode, leading to the chronic stage of AE.…”

Section: Biology and Immunology Of Susceptibility Versus Resistance Isupporting

confidence: 56%

Susceptibility versus resistance in alveolar echinococcosis (larval infection with Echinococcus multilocularis)

Gottstein

Wang

Boubaker

et al. 2015

Veterinary Parasitology

View full text Add to dashboard Cite

Epidemiological studies have demonstrated that the majority of human individuals exposed to infection with Echinococcus spp. eggs exhibit resistance to disease as shown by either seroconversion to parasite--specific antigens, and/or the presence of 'dying out' or 'aborted' metacestodes, not including hereby those individuals who putatively got infected but did not seroconvert and who subsequently allowed no development of the pathogen. For those individuals where infection leads to disease, the developing parasite is partially controlled by host immunity. In infected humans, the type of immune response developed by the host accounts for the subsequent trichotomy concerning the parasite development: (i) seroconversion proving infection, but lack of any hepatic lesion indicating the failure of the parasite to establish and further develop within the liver; or resistance as shown by the presence of fully calcified lesions; (ii) controlled susceptibility as found in the "conventional" alveolar echinococcosis (AE) patients who experience clinical signs and symptoms approximately 5-15 years after infection, and (iii) uncontrolled hyperproliferation of the metacestode due to an impaired immune response (AIDS or other immunodeficiencies). Immunomodulation of host immunity toward anergy seems to be triggered by parasite metabolites. Beside immunomodulating IL-10, TGFβ-driven regulatory T cells have been shown to play a crucial role in the parasite-modulated progressive course of AE. A novel CD4+CD25+ Treg effector molecule FGL2 recently yielded new insight into the tolerance process in Echinococcus multilocularis infection.

show abstract

Section: Biology and Immunology Of Susceptibility Versus Resistance Isupporting

confidence: 56%

Susceptibility versus resistance in alveolar echinococcosis (larval infection with Echinococcus multilocularis)

Gottstein

Wang

Boubaker

et al. 2015

Veterinary Parasitology

View full text Add to dashboard Cite

show abstract

“…Furthermore, the chemical composition of cyst fluid was discussed in some detail (Neisser, 1877). Recent developments of the immunobiology of the Echinococcus infection are described in previous reviews (e.g., Heath, 1995;Lightowlers and Gottstein, 1995;Gottstein and Hemphill, 2008;Mejri et al, 2010;Siracusano et al, 2012;Zhang et al, 2012) and in Chapter "Immunology...".…”

Section: Echinococcosis In Humansmentioning

confidence: 99%

Historical Aspects of Echinococcosis

Eckert

Thompson

2017

Advances in Parasitology

View full text Add to dashboard Cite

“…Within the liver of the intermediate host, the oncosphere then undergoes a metamorphosis toward the bladder-like metacestode larval stage which grows infiltratively, like a malignant tumor, into the surrounding host tissue. During this process, the early Th1 response is gradually replaced by a Th2 response, dominated by interleukin (IL)-5 and IL-10 [4]. AE has a high case-fatality rate and is associated with severe morbidity.…”

Section: Introductionmentioning

confidence: 99%

EmTIP, a T-Cell Immunomodulatory Protein Secreted by the Tapeworm Echinococcus multilocularis Is Important for Early Metacestode Development

2014

View full text Add to dashboard Cite

BackgroundAlveolar echinococcosis (AE), caused by the metacestode of the tapeworm Echinococcus multilocularis, is a lethal zoonosis associated with host immunomodulation. T helper cells are instrumental to control the disease in the host. Whereas Th1 cells can restrict parasite proliferation, Th2 immune responses are associated with parasite proliferation. Although the early phase of host colonization by E. multilocularis is dominated by a potentially parasitocidal Th1 immune response, the molecular basis of this response is unknown.Principal FindingsWe describe EmTIP, an E. multilocularis homologue of the human T-cell immunomodulatory protein, TIP. By immunohistochemistry we show EmTIP localization to the intercellular space within parasite larvae. Immunoprecipitation and Western blot experiments revealed the presence of EmTIP in the excretory/secretory (E/S) products of parasite primary cell cultures, representing the early developing metacestode, but not in those of mature metacestode vesicles. Using an in vitro T-cell stimulation assay, we found that primary cell E/S products promoted interferon (IFN)-γ release by murine CD4+ T-cells, whereas metacestode E/S products did not. IFN-γ release by T-cells exposed to parasite products was abrogated by an anti-EmTIP antibody. When recombinantly expressed, EmTIP promoted IFN-γ release by CD4+ T-cells in vitro. After incubation with anti-EmTIP antibody, primary cells showed an impaired ability to proliferate and to form metacestode vesicles in vitro.ConclusionsWe provide for the first time a possible explanation for the early Th1 response observed during E. multilocularis infections. Our data indicate that parasite primary cells release a T-cell immunomodulatory protein, EmTIP, capable of promoting IFN-γ release by CD4+ T-cells, which is probably driving or supporting the onset of the early Th1 response during AE. The impairment of primary cell proliferation and the inhibition of metacestode vesicle formation by anti-EmTIP antibodies suggest that this factor fulfills an important role in early E. multilocularis development within the intermediate host.

show abstract

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

Cited by 29 publications

References 104 publications

Susceptibility versus resistance in alveolar echinococcosis (larval infection with Echinococcus multilocularis)

Susceptibility versus resistance in alveolar echinococcosis (larval infection with Echinococcus multilocularis)

Historical Aspects of Echinococcosis

EmTIP, a T-Cell Immunomodulatory Protein Secreted by the Tapeworm Echinococcus multilocularis Is Important for Early Metacestode Development

Contact Info

Product

Resources

About