A schizont-derived protein, TpSCOP, is involved in the activation of NF-κB in Theileria parva-infected lymphocytes

Theileria parva is a tick-transmitted intracellular protozoan parasite that causes East Coast fever, a fatal bovine lymphoproliferative disease. The molecular mechanisms that underlie host cell transformation by T. parva schizonts have been studied extensively, and it is known that the transcription factor NF-κB is activated in schizont–infected cells, which makes the T. parva-transformed cells resistant to apoptosis. However, the mechanism by which the parasite triggers the activation of NF-κB remains enigmatic. In the present study, we biochemically characterized a novel protein, which we termed TpSCOP, which is expressed in the schizont stage of T. parva. TpSCOP was shown to interact with F-actin in vitro. Expression of TpSCOP in a murine lymphocytic cell line resulted in the activation of NF-κB signaling pathways, leading to apoptosis resistance. The activation of MAPKs, including ERK and JNK, were also detected. Furthermore, the introduction of TpSCOP into T. parva-infected cells also enhanced the activation of NF-κB. This is the first report to demonstrate that parasite-derived molecule has the ability to activate the host NF-κB pathway. Based on these results, TpSCOP likely plays an important role in apoptosis inhibition during Theileria infection.