Host resistance in the brain against Toxoplasma gondii

Abstract

Interferon (IFN)-gamma-dependent, cell-mediated immunity plays the major role in resistance against development of toxoplasmic encephalitis (TE). Humoral immunity also participates in controlling Toxoplasma gondii in the brain. Resistance is operative under collaboration among T and B cells, IFN-gamma-producing non-T cells, microglia, astrocytes, and dendritic cells. A number of cytokines, including IFN-gamma, mediate interactions between these cells and activation of effector cells that prevent intracellular replication of the parasite. The L(d) gene confers resistance against development of TE in mice. In humans, the HLA-DQ1 and -DQ3 genes are involved in regulating the resistance and susceptibility. Since these genes are a part of the major histocompatibility complex, which regulates the immune responses, the regulation of the responses by these genes appears to be important for determining host resistance to this disease. Strains of T. gondii also affect development of TE. Genotypes of the parasite may be an important factor for determining development of TE.