Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604853
Title: Ninjurin
Author: Hutchinson, James Alexander
Awarding Body: University of Cambridge
Current Institution: University of Cambridge
Date of Award: 2003
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Abstract:
Cellular stresses, including infection and neoplastic transformation, elicit responses that culminate in either successful resolution of cellular damage and cell survival, or failure and apoptosis. Damaged or infected cells that escape programmed cell death are potentially harmful and can be the target of immunological reactions. It is proposed that there exist immunological determinants expressed at the cell surface by damaged, infected or effete cells as part of a generalised cellular stress response and that there are recognised by cells of the innate immune system. A bioinformatic approach identified Ninjurin 1 and a novel paralogue, Ninjurin 2, as candidate stress-inducible cell surface-expressed molecules. Ninjurin-specific reagents were generated and used to characterise Ninjurin 1 and Ninjurin 2 expression. Ninjurin and Ninjurin 2 were found to be expressed in Natural Killer cells and activated macrophages. Expression of Ninjurin 1 could be induced by cellular stress in cultured epithelial cell lines, and expression of both Ninjurin 1 and Ninjurin 2 was markedly elevated in squamos cell carcinomas of the cervix. The possible involvement of Ninjurin in NK cell target recognition was investigated in conventional 51Cr-release assays and the effects of Ninjurin1 ligation in a myelomonocytic cell line were investigated. The expression data presented in this thesis are consistent with the hypothesised function of Ninjurin1 and Ninjurin2 as markers of distressed cells, but the case that the Ninjurin molecules facilitate the interaction of stressed cells with macrophages or NK cells is not yet proven.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.604853  DOI: Not available
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