CTLA-4 blockade augments human T lymphocyte-mediated suppression of lung tumor xenografts in SCID mice
dc.contributor.author | Sabel, Michael S. | en_US |
dc.contributor.author | Chen, Fang-An | en_US |
dc.contributor.author | Hess, Stephen D. | en_US |
dc.contributor.author | Egilmez, Nejat K. | en_US |
dc.contributor.author | Conway, Thomas F. | en_US |
dc.contributor.author | Bankert, Richard B. | en_US |
dc.date.accessioned | 2006-09-11T18:17:49Z | |
dc.date.available | 2006-09-11T18:17:49Z | |
dc.date.issued | 2005-10 | en_US |
dc.identifier.citation | Sabel, Michael S.; Hess, Stephen D.; Egilmez, Nejat K.; Conway, Thomas F.; Chen, Fang-An; Bankert, Richard B.; (2005). "CTLA-4 blockade augments human T lymphocyte-mediated suppression of lung tumor xenografts in SCID mice." Cancer Immunology, Immunotherapy 54(10): 944-952. <http://hdl.handle.net/2027.42/46864> | en_US |
dc.identifier.issn | 1432-0851 | en_US |
dc.identifier.issn | 0340-7004 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/46864 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=15846492&dopt=citation | en_US |
dc.description.abstract | Previous studies by others using transplantable murine tumor models have demonstrated that the administration of antibodies that block CTLA-4 interaction with B7 can provoke the elimination of established tumors, and that the tumor suppression is mediated by T-cells and/or cells expressing NK1.1. Studies from our lab have established in a human/severe combined immunodeficient (SCID) mouse chimeric model that autologous peripheral blood leukocytes (PBL) can suppress the growth of tumor xenografts in a PBL dose-dependent fashion, and that this suppression is dependent upon the patient’s T and NK cells. Using this human/mouse chimeric model, we sought to determine whether an antibody blockade of CTLA-4 would enhance the anti-tumor response of a patient’s PBL. It was first important to determine whether the tumor suppression observed in the SCID model was dependent upon CD28/B7 co-stimulation. Blockade of B7 with a human CTLA-4-Ig fusion protein completely abrogated the lymphocyte-mediated tumor suppression, confirming in this model that tumor suppression is dependent upon a CD28/B7 co-stimulation. Using two different CTLA-4 specific monoclonal antibodies, we observed that CTLA-4 blockade significantly enhanced the human lymphocyte-mediated tumor suppression in mice co-engrafted with PBL and tumor cells. This enhancement was observed in both an allogeneic setting (in which the PBL were allogeneic with respect to the tumor) and an autologous setting (in which the PBL and tumor were from the same patient). These results sustain the notion that human anti-tumor immune response can be augmented (in vivo) by blocking the interaction between CTLA-4 and B7. | en_US |
dc.format.extent | 360180 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Springer-Verlag | en_US |
dc.subject.other | SCID Mice | en_US |
dc.subject.other | Human CTLA-4 | en_US |
dc.subject.other | Medicine | en_US |
dc.subject.other | Lymphocytes | en_US |
dc.subject.other | Xenografts | en_US |
dc.title | CTLA-4 blockade augments human T lymphocyte-mediated suppression of lung tumor xenografts in SCID mice | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Microbiology and Immunology | en_US |
dc.subject.hlbsecondlevel | Biological Chemistry | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Surgery, 3304 Cancer Center, University of Michigan, 1500 East Medical Center Drive, Ann Arbor, MI, 48109, USA | en_US |
dc.contributor.affiliationother | Department of Otolaryngology, Division of Head and Neck Surgery, NYU Medical Center, New York, NY, 10016, USA | en_US |
dc.contributor.affiliationother | Department Of Microbiology and Immunology, Dartmouth Medical School, Lebanon, NH, 03756, USA | en_US |
dc.contributor.affiliationother | Department of Microbiology, State University of NY at Buffalo, Buffalo, NY, 14214, USA | en_US |
dc.contributor.affiliationother | Department of Microbiology, State University of NY at Buffalo, Buffalo, NY, 14214, USA | en_US |
dc.contributor.affiliationother | Department of Microbiology, State University of NY at Buffalo, Buffalo, NY, 14214, USA | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 15846492 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/46864/1/262_2005_Article_668.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/s00262-005-0668-3 | en_US |
dc.identifier.source | Cancer Immunology, Immunotherapy | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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