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dc.contributor.authorCHAPDELAINE, JOAN MARY
dc.date.accessioned2018-07-12T18:10:04Z
dc.date.available2018-07-12T18:10:04Z
dc.date.issued1981
dc.identifier.citationSource: Dissertation Abstracts International, Volume: 42-04, Section: B, page: 1384.
dc.identifier.urihttps://yulib002.mc.yu.edu/login?url=http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqm&rft_dat=xri:pqdiss:8120911
dc.identifier.urihttps://hdl.handle.net/20.500.12202/2737
dc.description.abstractCytotoxic T lymphocytes (CTL) generated during a murine sarcoma virus (MSV) infection have been found to be specific for both viral and H-2 antigens. Thus, in order for a target cell to be killed, it must express the same H-2 antigens as the CTL (H-2 restriction). Specifically, CTL recovered from primary MSV-induced tumors and spleens of H-2('b) mice are specific for the H-2D('b) molecule recognized in association with a viral antigen shared by the Friend, Moloney and Rauscher (FMR) viruses. The MSV-induced tumors also contain primed CTL precursor cells which, when restimulated in vitro, have the same specificity as the active cytotoxic T cells.;The H-2D('b) specificity has now been studied using a mutant cell line. A Friend virus-induced tumor cell line originating from a heterozygous H-2('b)/H-2('d) mouse was mutagenized with ethyl methanesulfonate (EMS). These cells were then treated with a hybridoma antibody directed against the H-2D('b) molecule in the present of rabbit complement. The surviving cells were no longer susceptible to the hybridoma antibody but were still lysed with conventional anti-H-2D('b) alloantiserum plus complement. Data obtained by sequential immunoprecipitation followed by gel electrophoresis indicate that both antisera recognized the same molecule. When the mutant cells were used as targets for H-2D('b)FMR specific CTL, the amount of cell lysis, compared to that seen with the nonmutant parent cells, was drastically decreased. However, they remain susceptible to allogeneic CTL raised against the H-2D('b) molecule. The mutant cells also did not differ from the parent cells in their level of viral antigen expression. Comparative tryptic peptide maps indicated that the H-2D('b) molecules from the parental and mutant cells were similar but not identical.;These studies suggest that a possible mechanism of escape by virus-infected cells from destuction by CTL might be alteration by somatic mutation of the Class I H-2 glycoprotein(s) that must be recognized by the CTL in order for them to be effective.
dc.publisherProQuest Dissertations & Theses
dc.subjectImmunology.
dc.titleSTUDIES OF TARGET CELL RECOGNITION BY CYTOTOXIC T LYMPHOCYTES
dc.typeDissertation


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