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In This Issue, The Journal of Immunology, Volume 171, Issue 3, August 2003, Pages 1121–1122, https://doi.org/10.4049/jimmunol.171.3.1121
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Turning off apoptosis
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Theileria parva, the parasite that causes East Coast fever in cattle, induces lymphoproliferation in the host. Although T. parva-infected T cells are activated, they escape activation-induced cell death by an unknown mechanism. Kūenzi et al. (p. 1224 ) looked at activation markers in parasite-infected bovine cells and in infected bovine cells that had been cured by treatment with the naphthoquinone derivative BW720c. Although procaspases 8 and 9 were detected in T. parva-infected cells, they were not cleaved until after 2 days of BW720c treatment. Infected and cured cells expressed Fas and FasL on their surfaces, but only the cured cells underwent apoptosis via induction of caspase activity. High levels of expression of FLIP and three other inhibitors of the caspase pathway were detected in T. parva-infected cells. By the third day of BW720c treatment of the infected cells, no inhibitor proteins could be found, indicating that expression of the anti-apoptotic proteins in the infected cells was highly dependent on the presence of the parasite. The findings demonstrate that T. parva is able to usurp anti-apoptotic proteins to render the cell resistant to apoptosis, thereby guaranteeing that its refuge is not destroyed.
