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Immune response to Echinococcus multilocularis infection in the mouse model: a review
1Dept. of Veterinary Parasitology, Faculty of Veterinary Medicine, Hokkaido University, Sapporo, Japan.
The Japanese Journal of Veterinary Research
|September 1, 1992
Summary
Cell-mediated immunity (CMI) suppresses Echinococcus multilocularis larval growth. Host resistance to this parasitic cestode infection correlates with T lymphocyte function, not antibody levels.
Area of Science:
- Parasitology
- Immunology
- Helminthology
Background:
- Echinococcus multilocularis is a parasitic cestode causing hydatid disease in humans and other intermediate hosts.
- Larval development in intermediate hosts leads to organ dysfunction and potential mortality.
- Mice are a common experimental model for studying E. multilocularis infections.
Purpose of the Study:
- To review larval Echinococcus multilocularis infection in mice.
- To detail the immune response to E. multilocularis infection.
- To investigate the role of cell-mediated immunity (CMI) in controlling larval growth.
Main Methods:
- Review of existing literature on larval E. multilocularis infection in mice.
- Analysis of immune responses in different mouse strains with varying T lymphocyte functions.
- Examination of immunosuppression markers associated with infection.
Main Results:
- Cell-mediated immunity (CMI) appears to significantly suppress larval E. multilocularis growth.
- Mice lacking thymocytes (nude mice) or with depleted thymocytes showed increased susceptibility.
- Mice strains with high helper T lymphocyte function exhibited resistance to infection.
- Antibody response levels did not correlate with susceptibility to E. multilocularis.
- Infection led to immunosuppression, including impaired cell function and reduced T lymphocyte activity.
Conclusions:
- Cell-mediated immunity plays a crucial role in controlling Echinococcus multilocularis larval development.
- T lymphocyte function is a key determinant of host resistance.
- Echinococcus multilocularis infection induces a state of immunosuppression in the host.
