Cellular immune recognition of HLA-G-expressing choriocarcinoma cell line Jeg-3.
dc.contributor.author | Burt, Deborah J | |
dc.contributor.author | Johnston, Diane | |
dc.contributor.author | Rinke de Wit, T | |
dc.contributor.author | Van den Elsen, P | |
dc.contributor.author | Stern, Peter L | |
dc.date.accessioned | 2010-06-11T11:36:47Z | |
dc.date.available | 2010-06-11T11:36:47Z | |
dc.date.issued | 1991 | |
dc.identifier.citation | Cellular immune recognition of HLA-G-expressing choriocarcinoma cell line Jeg-3. 1991, 6:117-22 Int. J. Cancer Suppl. | en |
dc.identifier.issn | 0898-6924 | |
dc.identifier.pmid | 2066177 | |
dc.identifier.uri | http://hdl.handle.net/10541/104714 | |
dc.description.abstract | Jeg-3 choriocarcinoma cells express class-I MHC HLA-G and low levels of a novel HLA-C product. The functional significance of such novel MHC class-I expression in regard of the cellular immune response has been investigated. Jeg-3 cells are NK-insensitive, but susceptible to LAK cytotoxicity, some of which is mediated by T cells. No Jeg-3-specific CTL or proliferative responses could be generated in allogeneic responder PBMC from several different donors. There was no detectable xenogeneic recognition of Jeg-3 cells even when preceded by in vivo priming. Jeg-3 cells are able to suppress proliferative responses in humans and others species. This is not reproduced by conditioned medium from the Jeg-3 cells, but can be overridden by IL-2. The ability of the Jeg-3 choriocarcinoma (trophoblast) cells to suppress in the MLR may reflect the processes which are shared to enable the survival of the foetus in a semi-allogeneic mother or a tumour in its host. It is not clear whether there is any relationship between the unusual class-I-MHC expression by trophoblast and the putative regulatory properties of the latter. | |
dc.language.iso | en | en |
dc.subject | Cancer Transplantation | en |
dc.subject.mesh | Animals | |
dc.subject.mesh | Cell Line | |
dc.subject.mesh | Choriocarcinoma | |
dc.subject.mesh | Cytotoxicity, Immunologic | |
dc.subject.mesh | DNA Replication | |
dc.subject.mesh | HLA Antigens | |
dc.subject.mesh | Histocompatibility Antigens Class I | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Killer Cells, Lymphokine-Activated | |
dc.subject.mesh | Killer Cells, Natural | |
dc.subject.mesh | Lymphocyte Activation | |
dc.subject.mesh | Mice | |
dc.subject.mesh | Neoplasm Transplantation | |
dc.subject.mesh | T-Lymphocytes | |
dc.subject.mesh | T-Lymphocytes, Cytotoxic | |
dc.subject.mesh | Teratoma | |
dc.subject.mesh | Transplantation, Heterologous | |
dc.title | Cellular immune recognition of HLA-G-expressing choriocarcinoma cell line Jeg-3. | en |
dc.type | Article | en |
dc.contributor.department | Cancer Research Campaign Department of Immunology, Paterson Institute for Cancer Research, Christie Hospital and Holt Radium Institute, Manchester, UK. | en |
dc.identifier.journal | International Journal of Cancer. Supplement | en |
html.description.abstract | Jeg-3 choriocarcinoma cells express class-I MHC HLA-G and low levels of a novel HLA-C product. The functional significance of such novel MHC class-I expression in regard of the cellular immune response has been investigated. Jeg-3 cells are NK-insensitive, but susceptible to LAK cytotoxicity, some of which is mediated by T cells. No Jeg-3-specific CTL or proliferative responses could be generated in allogeneic responder PBMC from several different donors. There was no detectable xenogeneic recognition of Jeg-3 cells even when preceded by in vivo priming. Jeg-3 cells are able to suppress proliferative responses in humans and others species. This is not reproduced by conditioned medium from the Jeg-3 cells, but can be overridden by IL-2. The ability of the Jeg-3 choriocarcinoma (trophoblast) cells to suppress in the MLR may reflect the processes which are shared to enable the survival of the foetus in a semi-allogeneic mother or a tumour in its host. It is not clear whether there is any relationship between the unusual class-I-MHC expression by trophoblast and the putative regulatory properties of the latter. |