QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

Help viewing high resolution images Return to article

Fig. 8. A model representing the modulation of NF-B-dependent gene expression by T. gondii. (A) Early in infection, the parasite triggers activation of the host IKK complex, resulting in a primary wave of NF-B translocation and induction of gene expression (early phase). An increase in TgIKK activity at the PVM phosphorylates a subset of IB molecules, inducing a secondary wave of NF-B activation (intermediate phase). The extent of this response is abrogated owing to a disruption in the host IKK signalosome. The magnitude of the NF-B transcriptional response might also depend on an amplification loop through autocrine effectors (i.e. TNF-, IL-1), resulting in sustained levels of gene expression at late stages of infection (late phase). (B) Signals deriving from the host IKK signalosome and TgIKK affect the strength and duration of the NF-B-dependent transcriptional response. Levels of gene expression shown in the blue line are for representation purposes only and do not reflect actual quantitative data. The regulation of specific NF-B target genes displays oscillatory patterns early in infection (blue line, early phase). An increase in TgIKK activity at the PVM (green dashed line) causes an activation of the response during mid-infection, resulting in sustained levels of NF-B-dependent gene expression (blue line, intermediate-to-late phases). An impaired IKK complex in the host cell abrogates this response significantly owing to a failure to attain an `activation threshold' (black dashed line) required by TgIKK for the induction of sustained levels of NF-B activation (orange line).

Return to article