HMGB1 is highly conserved with.98% amino acid identity between humans and rodents, but appears to be more polymorphic among parasite Nefiracetam species. Mammalian HMGB1 bears two DNA binding motifs followed by an acidic C-terminus, whereas most HMGB1 family members of parasites have only one or more HMG box and no acidic tail. T. gondii is an obligate intracellular protozoan that can actively invade almost all nucleated cells and can cause opportunistic disease in various animals and humans. The pathological basis for Toxoplasmosis is tissue destruction and inflammation, which are a direct result of the parasite��s cell lytic growth cycle of attachment, invasion, growth, and egress. There are three T. gondii genotypes, types I, II, and III, which have different growth characteristics and cause variable levels of virulence in mice. Type I strains are uniformly lethal at all doses in all strains of laboratory mice, whereas type II and type III show much lower levels of pathogenicity. Virulence in type I strains is a result of rhoptry effector proteins effectively eliminating critical host immune responses which leads to uncontrolled proliferation of the tachyzoite, and host survival is compromised due to excessive parasite burden. Type II strains induce stronger proinflammatory responses, including very high levels of IL-12 in comparison with either type I or III and the susceptible animals VX-745 always die of severe inflammation. Like type I, Type III strains limit the initial production of pro-inflammatory cytokines, whereas be unable to avoid intracellular killing mediated by IRGs and late production of IL-12 by DCs triggers a Th1-type response that is sufficient to control parasite burden and induce cyst formation, leading to a chronic infection. The transitions between the different stages of the T. gondii life cycle allow the parasite to be virulent and survive. These developmental transitions are accompanied by major changes in gene expression, and the control mechanisms for parasite proliferation may be regulated by the cell cycle and the micro-environments around the parasites. Regulation of T. gondii gene expression is, in part, promoted by epigenetic events, such as histone modifications and interactions between histones and other nuclear factors.