Immunology

Antibody and cell-mediated immunity are both elicited by T. gondii infection. The role of antibody in the control of the infection is secondary to the effects of the cell-mediated immune response. A balance between innate and adaptive mechanisms leads to proinflammatory and regulatory responses in the immunopathol-ogy of toxoplasmosis (Alexander and Hunter, 1998). Cell-mediated production of Thl responses that limit Toxoplasma growth must be controlled to limit host damage. Several cell types are responsible for controlling intracellular growth of T. gondii (Suzuki, 1999). T lymphocytes of CD8 + , CD4 + and y8 specificity, as well as macrophages, dendritic cells and neutrophils, are important in creating and maintaining the Thl response (Denkers and Gazzinelli, 1998). The immune reaction to T. gondii infection also involves depression of parts of the immune machinery (Channon and Kasper, 1996). Micro-neme and surface antigens of T. gondii trigger monocytes to downregulate mitogen-induced lymphoproliferation (Channon et al., 1999). Experimental animal studies involving the natural oral route of infection have revealed the importance of gut immunity in the acute stages of toxoplasmosis. Intraepithelial CD8+ lymphocytes isolated from infected mice can be shown to provide long-term protection against infective challenge (Lepage et al., 1998). The lymphokines that are known to be important in host protection include interferon (IFN) gamma (IFNy), tumor necrosis factor alpha (TNFa) and nitric oxide, which have been shown to be key components in anti-Toxoplasma responses. While these are unquestionably necessary, they may not explain all aspects of parasite control. IFN and TNFa stimulation of non-immune effector cells to kill T. gondii may not be completely dependent on nitric oxide production

Fig. 5.7 Electron micrograph of two intracellular T. gondii that are each beginning the second round of division by endodyogeny, as shown by the formation of daughter apical complexes (D) within each parent. Several apical organelles, including dense granules (dg), micronemes (mn) and rhoptries (rh), are seen within the parents. The parasitophorous vacuole space is filled with the tubulovesicular network (tvn), which is thought to function in parasite salvage of host metabolites. A host mitochondrion (mt) is seen at the edge of the parasitophorous vacuole. The host lysosomal compartments (ly) are labeled by graular thorium dioxide, showing that none of these bodies fuse with the parasitophorous vacuole. Magnification x 10000

Fig. 5.7 Electron micrograph of two intracellular T. gondii that are each beginning the second round of division by endodyogeny, as shown by the formation of daughter apical complexes (D) within each parent. Several apical organelles, including dense granules (dg), micronemes (mn) and rhoptries (rh), are seen within the parents. The parasitophorous vacuole space is filled with the tubulovesicular network (tvn), which is thought to function in parasite salvage of host metabolites. A host mitochondrion (mt) is seen at the edge of the parasitophorous vacuole. The host lysosomal compartments (ly) are labeled by graular thorium dioxide, showing that none of these bodies fuse with the parasitophorous vacuole. Magnification x 10000

(Yap and Sher, 1999a,b), neither does the long-term immunity induced by vaccination rely on nitric oxide, although it is IFN-dependent (Khan, Matsuura and Kasper, 1998). Dendritic cells may be important in the immune response to re-exposure to T. gondii. Lymphocytes from donors with evidence of previous toxoplasmosis induced rapid and strong production of interleukin 12 (IL-12) from human dendritic cells, which would be expected to produce a rapid burst of IFNy (Seguin and Kasper, 1999).

The effective and balanced immune response of immunocompetent individuals controls the infection, in most cases causing little organ damage, but does not eradicate the infection. The bradyzoite cysts elicit little immune reaction and may persist for the life of the host. Changes in the host's immune functions may allow reactivation of actively replicating tachyzoites which must be controlled by further cellmediated mechanisms. If the host is incapable of mounting or regulating this response, the outcome is extensive organ damage.

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