| 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]
[246] |
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]. |
