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Review
. 2003 Nov;71(11):6109-15.
doi: 10.1128/IAI.71.11.6109-6115.2003.

Apoptosis and the balance of homeostatic and pathologic responses to protozoan infection

L Cristina Gavrilescu  1 , Eric Y Denkers
Affiliations
Review

Apoptosis and the balance of homeostatic and pathologic responses to protozoan infection

L Cristina Gavrilescu et al. Infect Immun. 2003 Nov.
No abstract available

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Figures (V体育安卓版)

FIG. 1.
FIG. 1.
PCD induced through multiple pathways. After cleavage and activation (green arrows) of the initiator Casp-8 and -9, the caspase cascade leads to cell death through further activation of death effector molecules. (A) Receptor-mediated induction of apoptosis. Extracellular molecules (TNF-α and FasL) bind to TNFR family members (TNFR I and Fas, respectively). Recruitment of FADD to the receptors leads to Casp-8 activation, which in turn results in activation of Casp-3, -6, and -7. (B) Stress, irradiation, and inflammation act on mitochondria through intermediary proapoptotic Bcl-2 family members such as Bax, resulting in blocking of the antiapoptotic activity of Bcl-2 (red lines). As a result of the latter event, cytochrome c translocates into the cytoplasm and activates Casp-9 through APAF-1. Casp-8 may also trigger the mitochondrial PCD pathway through activation of Bid, which, like Bax, inhibits the antiapoptotic activity of Bcl-2. (C) Cytotoxic cells introduce granzyme molecules into the target cell in a process mediated by multimerization of the perforin molecule. Granzymes cleave various substrates, including caspases, resulting in cell death. The dashed arrows indicate secondary effects of activated caspases. PARP, poly(ADP-ribose) polymerase; MAPK, mitogen-activated protein kinase.
FIG. 2.
FIG. 2.
Apoptosis during protozoan infection. From the host perspective, CTL activity and AICD can be viewed as homeostatic, anti-inflammatory responses to protozoan parasite infection that control the spread of infection and resolve the immune response after resolution of the infection. Alternatively, overexpression of type 1 proinflammatory cytokines, nitric oxide, or Fas-FasL may lead to uncontrolled apoptosis, in this situation becoming a proinflammatory response. A switch from a homeostatic response to a pathological response may occur in the course of infection, as when type 1 cytokines act to limit infection but then cause tissue and cellular apoptotic damage.
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