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DC Field | Value | Language |
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dc.contributor.advisor | Underdown, Brian J. | en_US |
dc.contributor.author | Skea, Lynn Danna | en_US |
dc.date.accessioned | 2014-06-18T16:36:22Z | - |
dc.date.available | 2014-06-18T16:36:22Z | - |
dc.date.created | 2010-06-10 | en_US |
dc.date.issued | 1989-08 | en_US |
dc.identifier.other | opendissertations/1937 | en_US |
dc.identifier.other | 2964 | en_US |
dc.identifier.other | 1353280 | en_US |
dc.identifier.uri | http://hdl.handle.net/11375/6632 | - |
dc.description.abstract | <p>Giardia muris is an intestinal parasite of mice. It has a simple life cycle and is non-invasive. Therefore, G. muris infection provides a model to study immune mechanisms that operate at mucosal surfaces. Immunocompetent mice eliminate primary G. muris infections. T cell-dependent humoral immune mechanisms are involved in this process.</p> <p>The CBA/N mouse bears an X-linked immunodeficiency gene (Xid), the expression of which results in defective B cell maturation and consequent impairment of certain humoral immune responses. The antibody responses of CBA/N mice are particularly defective in certain isotypes and specificities.</p> <p>CBA/N mice fail to eliminate G. muris. The major focus of this dissertation was an attempt to elucidate the basis for chronic giardiasis in this strain.</p> <p>Cellular reconstitution experiments showed that the ability to eliminate G. muris was transferred to CBA/N mice with lymphoid cells from immunocompetent, CBA/Ca mice. Reconstitution required prior irradiation of recipient mice, and was not effective with semi-purified B cells and T cells. These results indicate that conventional B cells and T cells are insufficient, and that another cell type is also required. This cell may be the Lyl+ B cell.</p> <p>CBA/N mice make quantitatively deficient serum IgG antibody responses to G. muds infection. Providing CBA/N mice with this antibody failed to induce elimination of the parasite, thus this isotype defect was ruled out as the cause of their susceptibility to chronic giardiasis.</p> <p>Analysis of G. muris antigen recognition failed to reveal a specificity defect in the antibody response of CBA/N mice. However, a glycolipid component of G. muris bound serum IgM from CBA/J and BALB/c mice, but not serum IgM from CBA/N mice. These results indicate a possible structural defect in IgM from CBA/N mice.</p> <p>Although unable to eliminate primary G. muris infection, drug-cured CBA/N mice are resistant to reinfection. These results indicate that the immune mechanisms that mediate elimination of G. muris are different from those that mediate resistance to reinfection.</p> | en_US |
dc.subject | Medical Sciences | en_US |
dc.subject | Medical Sciences | en_US |
dc.title | Chronic Giardiasis in CBA/N Mice: Use of Genetically Immunodeficient Mice to Study Mechanisms of Immunity to an Intestinal Parasite | en_US |
dc.type | thesis | en_US |
dc.contributor.department | Medical Sciences | en_US |
dc.description.degree | Doctor of Philosophy (PhD) | en_US |
Appears in Collections: | Open Access Dissertations and Theses |
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fulltext.pdf | 6.72 MB | Adobe PDF | View/Open |
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