Contribution of T-cell responses to immunity and pathogenesis in infection with Theileria parva

Abstract

The importance of T-cell-mediate immune responses in the control of intracellular protozoan parasites is now well established 1-3. The killing of parasitized cells by T cells and cytokine-mediated effects on growth and viability of the intracellular parasites have both been implicated as effector mechanisms2-8. At the same time, it is clear that the induction of inappropriate T-cell responses may result in not only a failure to control infection, but also an enhanced severity of disease. This is best documented for infecitons with Leishmania in mice 2,9. The bovine protozoan parasite, Theileria parva (see box 1), presents an intriguing challenge to the immune system in that it infects lymphocytes and modifies their phenotype and behaviour. The parasite has evolved a unique relationship with host lymphocytes whereby development from the sporozoite to the schizont causes activation and proliferation of the host cell. By dividing at the same time as the transformed lymphocyte, parasites multiply by clonal expansion of the infected cell population 10,13. Hence there is the potential to influence parasite replication both at the level of the parasite and of the host cell. Given that activated lymphoid cells may express receptorsw for cytokines, some of which act as growth factors, products of T-cell responses elicited by the parasite may have either positive or negative effects on the growth of parasitized cells. Studies of the immune responses of cattle immunized against T. parva have shown parasite-specific CD4+ and CD8+ T-cell responses against infected lymphocytes 3,4,18,19.