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Figure 2

Figure 2. From: Discrimination between Host and Pathogens by the Complement System.

Host/target discriminatory sites on factor H. While the N-terminal four domains express all of the complement regulatory functions of factor H, this activity is controlled by other polyanion and C3b binding sites localized to domains 7, 12–13 and 19–20, as indicated. Interactions between these sites and host cell surface polyanion markers increases the effectiveness of the complement regulating domains 1–4 thus preventing inappropriate complement activation on host cells and tissues. Microorganisms lacking molecules recognized by factor H cannot control activation of the alternative complement pathway on their surface.

Michael K. Pangburn, et al. Vaccine. ;26(Suppl 8):I15-I21.
Figure 3

Figure 3. From: Discrimination between Host and Pathogens by the Complement System.

The specificity of the reactive thioester site of C3 for carbohydrates can determine the rate and extent of complement activation. Different strains of yeast (Cryptococcus neoformans) capable of attaching different numbers of xylose residues per unit of surface polysaccharide exhibit different rates and extents of complement activation [49]. The serotypes attach one (52D), two (271A), three (182B) or four (191C) xylose terminal residues to surface oligosaccharides during growth. The figure shows deposition of radiolabeled C3b on the organisms during activation of the alternative pathway revealing a 2-fold difference in rate of activation and a 4-fold difference in the level of opsonization by C3b. Figure from [49] with permission.

Michael K. Pangburn, et al. Vaccine. ;26(Suppl 8):I15-I21.
Figure 1

Figure 1. From: Discrimination between Host and Pathogens by the Complement System.

Complement activation occurs through one or more of three distinct pathways. The primary targets of each pathway (i.e., the molecular structures that activate that pathway) are different. Each pathway employs a unique set of discriminatory molecules. Some, such as factor H of the alternative pathway, recognize markers on host cells to prevent activation on the host, but allow activation on most other surfaces. Other discriminatory molecules recognize target molecules using pattern recognition mechanisms (properdin, MBL, ficolins, C1q and SIGN-R1) capable of interacting with target surface molecules. Discriminatory specificity developed in the adaptive immune system and expressed in the form of antibodies is utilized by the classical pathway to identify targets for activation of this pathway. All activation pathways lead to C3b attachment to the target and the specificity of the thioester reactive site influences the rate and extent of the activation process. Finally, targets of complement activation undergo numerous processes all directed either at killing or at developing lasting immunity.

Michael K. Pangburn, et al. Vaccine. ;26(Suppl 8):I15-I21.

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