Abstract
Human, polyclonal, nonspecific IgG labeled with 111In has shown clinical utility for inflammation detection1, but the process by which 111In localizes in an abscess is little understood. While breakdown in the endothelial barrier may explain the initial localization process, it cannot explain the retention over 24 or 48 hr of the clinical time frame. We have suggested that factors at the abscess site, e.g., high concentrations of Lactoferrin (LF) or Ferritin (FE) and low molecular weight mediators e.g., ATP, permit 67Ga to be translocated to these proteins and aid in the continual accumulation of radionuclide2,3. This general model can be applied to the localization of 111In-IgG and is shown in Figure 1. In this study we have examined the details of the transfer of 114mln from IgG-DTPA to LF and transferrin (TF).
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© 1994 Springer Science+Business Media New York
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Carlson, A.J., Sasso, D., Weiner, R.E. (1994). Transchelation of 114mIn from IgG-DTPA to Abscess-Related Proteins. In: Martin-Comin, J., Thakur, M.L., Piera, C., Roca, M., Lomeña, F. (eds) Radiolabeled Blood Elements. NATO ASI Series, vol 262. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2462-5_3
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DOI: https://doi.org/10.1007/978-1-4615-2462-5_3
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