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The discovery comes from researchers at the University of Virginia in the US, whose tests on lab mice showed that important brain defenders, but the researchers suggest that the parasite may hitch a ride inside T cells to create a kind of Trojan horse – enabling it to spread further.
That's when the infected immune cells take drastic action."T cells can destroy infected cells or cue other cells to destroy the parasite. We found that these very T cells can get infected, and, if they do, they can opt to die.parasites need to live inside cells, so the host cell dying is game over for the parasite." Four weeks after infection, mice without caspase-8 showed higher levels of inflammation than animals with caspase-8 . Arrows indicate inflamed blood vessels, and arrowheads indicate. While caspase-8 was already known to be important to the immune system and cell death, its role here – specifically in cells known as CD8from both the mice with caspase-8, and those without it. The bodies of all of the animals were still working hard to fight off the infection, but some lacked a vital defensive mechanism.actually attempts this T cell trick– and that's quite possibly because of the self-destruct mechanism that caspase-8 manages. For pathogens to survive, they need to interfere with caspase-8 somehow.Caspase-8 leads to T cell death. The only pathogens that can live in CD8+ T cells have developed ways to mess with Caspase-8 function.Most people won't know they've got toxoplasmosis and will recover on their own, and this study gives us a good idea why. However, the parasite can cause problems for those who are pregnant or who have a weakened immune system – if they'rebased on this new information, although we've only seen its effects in mice so far. More broadly, scientists now have a better understanding of the function of CD8"People with compromised immune systems are vulnerable to this infection, and now we have a better understanding of why and how we can help patients fight this infection."
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