Modulation of Host Programmed Cell Death Pathways by the Intracellular Protozoan Parasite, Toxoplasma gondii — Implications for Maintenance of Chronic Infection and Potential Therapeutic Applications

摘要: Programmed cell death (PCD) pathways are genetically programmed mechanisms that can trigger the to die or commit “cell suicide”. There three major forms of pro‐ grammed now recognized: apoptosis (type I), autophagy II) and necrotic necroptosis III). While these processes were once thought occupy discrete states, evidence suggests apoptosis, necrosis often regulated by similar share initiator effector mole‐ cules some subcellular compartments indicating crosstalk exists between main pathways, resulting in a balanced interplay which decides its fate. PCD have important roles many cellular such as development oncogenic transformation, but also play host defense elimination pathogens. Toxoplasma gondii is microbial patho‐ gen for key part defense. T. gon‐ dii an obligate intracellular protozoan parasite infects approximately one-third world’s population. In most immunocompetant individuals, chronic infection asymptomatic due effective immune response eliminates active repli‐ cation. The has evolved evasion strategies enable it survive persist long enough however establish cyst stage persists within neurons brain skeletal muscle periphery. multiple resist killing apoptotic, autophagic parasite’s manipulation plays cru‐ cial role host–parasite interactions maintenance infection. individuals chronically infected with asymptomatic, severe disease occur immunocompromised where reactivates from causing necrotizing encephalitis, increasing indicates cere‐ bral toxoplasmosis may lead neuropsychiatric disorders schizophrenia suicidal behavior. This review will focus on pathways. A bet‐ © 2015 Author(s). Licensee InTech. chapter distributed under terms Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), permits unrestricted use, distribution, reproduction any medium, provided original work properly cited. ter understanding molecular components underlying yield new therapeutic targets treatment clinical sequelae cerebral toxoplasmosis.