The factors that influence tissue cyst formation and induce differentiation of different stages are not known in detail. The transition from tachyzoite to bradyzoite is followed by a shift in stage-specific antigens (Bohne et al. 1993). Nitric oxide production by T. gondii-infected macrophages seem an important mediator in reducing parasite multiplication and initiation of bradyzoite formation (Bohne et al. 1994).
Tissue cysts are more numerous in animals in the chronic stage of infection with developed immunity than in animals in the acute stage of infection, but tissue cysts have been found in mice infected for only three days (Dubey and Frenkel 1976) and in tissue cell culture systems not influenced by any immune mechanism (Lindsay et al. 1991, 1993). The role of the developing immune response in the formation of tissue cysts is therefore still undecided. The cyst contains both host-derived and T. gondii antigens (Sims et al. 1988). The factors that determine the rupture of the cyst are unknown. Parasites can be released by the calcium ionophore, monensin (Endo et al. 1982), which implicates a role of calcium. One theory is that cysts rupture from time to time and the released bradyzoites are destroyed by host immune response or give rise to new cysts or tachyzoites, depending on the immune status of the host. Chronic infection can be relapsed reliably in rodents by corticosteroids or by relapsing, depleting, or interfering with cytokine production (Gazzinelli et al. 1993).
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