The role of CD23+ B cells in host protection against Schistosoma mansoni

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Authors
Hauslein, Elizabeth Ellen
Issue Date
2007
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Thesis
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en_US
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Abstract
Schistosomiasis caused by three main species of parasitic trematodes affects over 207 million people worldwide. Individuals who are resistant to reinfection with schistosomes have an increased percentage of CD23+ B cells, but it is currently unknown what role CD23 plays in host defense. CD23 is the low affinity IgE receptor (FCeRII) which has been shown to be involved in antigen presentation and the regulation of IgE production by B cells. We hypothesized that CD23 expression on B cells has a protective role in host immunity to schistosomes by enhancing IgE production. We first determined the anatomical distribution of CD23+ B cells from unexposedluninfected donors and the cellular phenotypes using flow cytometric methods and found that CD 19+ B cells in whole blood and tonsils express high levels ofCD23, and these B cell populations exist in different stages of activation and differentiation. We next assessed the effects of CD23-bound IgE on B cell activation and signaling using flow cytometric methods and Western blot analysis and found that the ability of B cells to bind exogenous IgE is directly related to the level ofCD23 and that NP-BSA induced a stronger signaling response at the level of BLNK whereas anit-IgE appears inhibit BLNK phosphorylation. Our pilot studies indicate that the mechanism by which CD23-bound IgE is cross-linked will determine the outcome of B cell development and ultimate IgE output. These results have allowed us to model the possible fates of CD23+ B cells for a better understanding of a potential role for these cells in human schistosomiasis, and gaining an understanding of the development and maintenance of immunological resistance to schistosomes will be beneficial in aiding in the development of a vaccination.
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v, 33 p.
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Kalamazoo College
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U.S. copyright laws protect this material. Commercial use or distribution of this material is not permitted without prior written permission of the copyright holder.
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