Evasion strategy Consequence(s) Molecular mechanism(s) Parasite effect References
Apoptosis of CD4+ cells T-cell unresponsiveness Cell death by neglect Indirect [237]
Apoptosis of leukocytesa Unrestricted parasite replication and host death Upregulation of Fas and FasL;
TNF-dependent mechanisms
Indirect [238-240]
Inhibition of apoptosis in parasite-positive cells Blockade of host cell suicide; avoidance of CTL- and NK-mediated cytotoxicity Inhibition of cytochrome c-release; upregulation of anti-apoptotic molecules
Interference with caspase activation; degradation of PARP (?)
Direct [241-245]      
CTL: Cytotoxic T lymphocyte; Fas: Receptor; FasL: Fas Ligand (a cell surface molecule belonging to TNF family and death factor, which binds to its receptor Fas, thus inducing apoptosis of Fas-bearing cells); NK: Natural Killer cells; PARP, Poly(ADP-Ribose) Polymerase. aT. gondii delayed neutrophil apoptosis by inducing granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor secretion by the parasite-infected human fibroblasts. Although neutrophils are unable to kill T. gondii, this can retard their division time from the usual 6-8 hrs cycle to a 24 hrs cycle and this enhanced neutrophil survival may contribute to the robust proinflammatory response elicited in the pathogen-infected host cells [247].
Table 10: Suppression of immune responses to T. gondii by parasite-triggered modulation of host cell apoptosis (acc. to Lang, Gro β & Lüder [231]; with own modification).