T-cell receptor gene rearrangement and expression in human natural killer cells: natural killer activity is not dependent on the rearrangement and expression of T-cell receptor α , β , or γ genes
dc.contributor.author | Bray, Robert A. | en_US |
dc.contributor.author | Kornbluth, Jacki | en_US |
dc.contributor.author | Landay, Alan L. | en_US |
dc.contributor.author | Strominger, Jack L. | en_US |
dc.contributor.author | Gebel, Howard | en_US |
dc.contributor.author | Seidman, Jon G. | en_US |
dc.contributor.author | Gottschalk, Lisa | en_US |
dc.contributor.author | Quertermous, Thomas | en_US |
dc.contributor.author | Coury, Larry | en_US |
dc.contributor.author | Gottesdiener, Keith M. | en_US |
dc.contributor.author | Leiden, Jeffrey M. | en_US |
dc.date.accessioned | 2006-09-11T18:09:10Z | |
dc.date.available | 2006-09-11T18:09:10Z | |
dc.date.issued | 1988-04 | en_US |
dc.identifier.citation | Leiden, Jeffrey M.; Gottesdiener, Keith M.; Quertermous, Thomas; Coury, Larry; Bray, Robert A.; Gottschalk, Lisa; Gebel, Howard; Seidman, Jon G.; Strominger, Jack L.; Landay, Alan L.; Kornbluth, Jacki; (1988). "T-cell receptor gene rearrangement and expression in human natural killer cells: natural killer activity is not dependent on the rearrangement and expression of T-cell receptor α , β , or γ genes." Immunogenetics 27(4): 231-238. <http://hdl.handle.net/2027.42/46745> | en_US |
dc.identifier.issn | 0093-7711 | en_US |
dc.identifier.issn | 1432-1211 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/46745 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=3346041&dopt=citation | en_US |
dc.description.abstract | To test the hypothesis that the T-cell receptor ( Tcr ) λ gene encodes a natural killer (NK) cell receptor molecule, three human NK clones and fresh peripheral blood lymphocytes with NK activity from two patients with a CD16 + lymphocytosis were analyzed for rearrangements and expression of the human Tcr α, β , and λ genes. Two of the clones displayed distinct rearrangements of their Tcr β and λ genes and expressed mature Tcr α, β , and αl RNA. However, one of the clones and both patient samples displayed marked NK activity but failed to rearrange or express any of their Tcr genes. These findings demonstrate that human natural killer activity is not dependent on Tcr λ gene rearrangement and expression. In addition, they confirm previous findings concerning the lack of Tcr α and β gene expression in some natural killer cells. Thus, they suggest the existence of additional NK-specific recognition molecules. | en_US |
dc.format.extent | 930868 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 | Biomedicine | en_US |
dc.subject.other | Allergology | en_US |
dc.subject.other | Immunology | en_US |
dc.subject.other | Cell Biology | en_US |
dc.title | T-cell receptor gene rearrangement and expression in human natural killer cells: natural killer activity is not dependent on the rearrangement and expression of T-cell receptor α , β , or γ genes | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Public Health | 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 | Division of Tumor Virology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA; Howard Hughes Medical Institute, University of Michigan Medical Center, 1150 West Medical Center Drive, MSRB I, Room 4510, 48109, Ann Arbor, MI, USA; Howard Hughes Medical Institute, University of Michigan Medical Center, 48109, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationother | Division of Tumor Virology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA | en_US |
dc.contributor.affiliationother | Division of Tumor Virology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA | en_US |
dc.contributor.affiliationother | Department of Genetics, Harvard Medical School, Boston, Massachusetts, USA | en_US |
dc.contributor.affiliationother | Division of Tumor Virology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA | en_US |
dc.contributor.affiliationother | Department of Immunology/Microbiology, Rush Presbyterian St. Luke's Medical Center, Chicago, Illinois, USA | en_US |
dc.contributor.affiliationother | Department of Immunology/Microbiology, Rush Presbyterian St. Luke's Medical Center, Chicago, Illinois, USA | en_US |
dc.contributor.affiliationother | Department of Immunology/Microbiology, Rush Presbyterian St. Luke's Medical Center, Chicago, Illinois, USA | en_US |
dc.contributor.affiliationother | Department of Genetics, Harvard Medical School, Boston, Massachusetts, USA | en_US |
dc.contributor.affiliationother | Department of Immunology/Microbiology, Rush Presbyterian St. Luke's Medical Center, Chicago, Illinois, USA | en_US |
dc.contributor.affiliationother | Department of Pathology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 3346041 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/46745/1/251_2004_Article_BF00376117.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/BF00376117 | en_US |
dc.identifier.source | Immunogenetics | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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