MIC1 and MIC3 : partners in invasion
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《实验药学杂志》
MIC3 (red) binds to the surface of host cells and facilitates Toxoplasma infection.
Adhesive proteins that are discharged from the parasite Toxoplasma gondii and grab onto target cells are needed for infection, according to a study on page 453. Cerede et al. removed two proteins from T. gondii and with it stripped the parasite of its virulence in mice.Microneme proteins MIC1 and MIC3 are soluble members of a family of parasitic adhesion proteins that are secreted from the parasite, based on an unknown trigger, and bind to the surface of host cells. These proteins are thought to facilitate binding of the parasite to host cells, but their contribution to virulence remains largely unexplored.
Deletion of both MIC1 and MIC3, Cerede et al. now show, prevents parasites from invading host cells and establishing infection in mice. Reexpression of either protein in the deficient parasite strain restored virulence. Mice exposed to the deficient strain of T. gondii were protected from later infection with wild-type parasites, suggesting that removal of MIC1 and MIC3 did not affect immunogenicity.
T. gondii can be transmitted to humans by ingestion of infected meat or cat feces–contaminated food and is a risk for pregnant women as it can cause congenital infections in the developing fetus. The authors suggest that this deficient strain could be used as a veterinary immunization, thereby preventing animal infections and limiting human exposure.
Adhesive proteins that are discharged from the parasite Toxoplasma gondii and grab onto target cells are needed for infection, according to a study on page 453. Cerede et al. removed two proteins from T. gondii and with it stripped the parasite of its virulence in mice.Microneme proteins MIC1 and MIC3 are soluble members of a family of parasitic adhesion proteins that are secreted from the parasite, based on an unknown trigger, and bind to the surface of host cells. These proteins are thought to facilitate binding of the parasite to host cells, but their contribution to virulence remains largely unexplored.
Deletion of both MIC1 and MIC3, Cerede et al. now show, prevents parasites from invading host cells and establishing infection in mice. Reexpression of either protein in the deficient parasite strain restored virulence. Mice exposed to the deficient strain of T. gondii were protected from later infection with wild-type parasites, suggesting that removal of MIC1 and MIC3 did not affect immunogenicity.
T. gondii can be transmitted to humans by ingestion of infected meat or cat feces–contaminated food and is a risk for pregnant women as it can cause congenital infections in the developing fetus. The authors suggest that this deficient strain could be used as a veterinary immunization, thereby preventing animal infections and limiting human exposure.