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Article: Rearrangements of T-cell receptor gene YT35 in human DNA from thymic leukaemia T-cell lines and functional T-cell clones

TitleRearrangements of T-cell receptor gene YT35 in human DNA from thymic leukaemia T-cell lines and functional T-cell clones
Authors
Issue Date1984
Citation
Nature, 1984, v. 311, n. 5984, p. 385-387 How to Cite?
AbstractAn essential property of the immune response is its ability to distinguish between self and non-self and to generate enormous diversity in antibody and T-cell immune responses. Although the genetic and molecular mechanisms responsible for antibody diversity have now largely been elucidated, the structure of the T-cell receptor and the diversification of the receptor repertoire have only recently become amenable to study. One approach has involved immunochemical studies of the protein precipitated by monoclonal antibodies which react specifically with the immunizing T-cell clones 1-3. Another approach has been to clone and sequence a human 4 or a murine5 T-cell specific message that may specify part of the T-cell receptor. We present here results of Southern blot analysis of non-T, immature T, and mature T-cell genomic DNA, and provide evidence that rearrangements of the YT35 sequences do occur in the DNA of thymic leukaemia T cells. This suggests that YT35 codes for at least part of the T-cell receptor and that rearrangements occur at this early stage of thymic ontogeny. Furthermore, DNA rearrangements are present in lymphocytes with phenotypic and functional characteristics of helper, killer, or suppressor T cells. We conclude that the three subpopulations of T cells operate via receptor molecules encoded by the same gene family. © 1984 Nature Publishing Group.
Persistent Identifierhttp://hdl.handle.net/10722/292281
ISSN
2023 Impact Factor: 50.5
2023 SCImago Journal Rankings: 18.509
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorToyonaga, Barry-
dc.contributor.authorYanagi, Yusuke-
dc.contributor.authorSuciu-Foca, Nicole-
dc.contributor.authorMinden, Mark-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:56:08Z-
dc.date.available2020-11-17T14:56:08Z-
dc.date.issued1984-
dc.identifier.citationNature, 1984, v. 311, n. 5984, p. 385-387-
dc.identifier.issn0028-0836-
dc.identifier.urihttp://hdl.handle.net/10722/292281-
dc.description.abstractAn essential property of the immune response is its ability to distinguish between self and non-self and to generate enormous diversity in antibody and T-cell immune responses. Although the genetic and molecular mechanisms responsible for antibody diversity have now largely been elucidated, the structure of the T-cell receptor and the diversification of the receptor repertoire have only recently become amenable to study. One approach has involved immunochemical studies of the protein precipitated by monoclonal antibodies which react specifically with the immunizing T-cell clones 1-3. Another approach has been to clone and sequence a human 4 or a murine5 T-cell specific message that may specify part of the T-cell receptor. We present here results of Southern blot analysis of non-T, immature T, and mature T-cell genomic DNA, and provide evidence that rearrangements of the YT35 sequences do occur in the DNA of thymic leukaemia T cells. This suggests that YT35 codes for at least part of the T-cell receptor and that rearrangements occur at this early stage of thymic ontogeny. Furthermore, DNA rearrangements are present in lymphocytes with phenotypic and functional characteristics of helper, killer, or suppressor T cells. We conclude that the three subpopulations of T cells operate via receptor molecules encoded by the same gene family. © 1984 Nature Publishing Group.-
dc.languageeng-
dc.relation.ispartofNature-
dc.titleRearrangements of T-cell receptor gene YT35 in human DNA from thymic leukaemia T-cell lines and functional T-cell clones-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/311385a0-
dc.identifier.pmid6332987-
dc.identifier.scopuseid_2-s2.0-0021226499-
dc.identifier.volume311-
dc.identifier.issue5984-
dc.identifier.spage385-
dc.identifier.epage387-
dc.identifier.isiWOS:A1984TK56000056-
dc.identifier.issnl0028-0836-

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