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Article: T cell receptor (TcR) β chain transgenic mice: Studies on allelic exclusion and on the TcR+ γ/δ population

TitleT cell receptor (TcR) β chain transgenic mice: Studies on allelic exclusion and on the TcR<sup>+</sup> γ/δ population
Authors
Issue Date1990
Citation
European Journal of Immunology, 1990, v. 20, n. 2, p. 417-424 How to Cite?
AbstractTo study allelic exclusion of TcR genes we analyzed two types (I and II) of TcR β transgenic mice. T cells derived from both types of mice contained similar amounts of transgenic RNA transcripts; however, surface expression of the transgenic β chain was drastically reduced in type II compared to type I. In type I transgenic mice, productive rearrangements and expression of endogenous TcR β genes were suppressed whereas on T cells of type II mice, both transgenic and endogenous TcR β chains were expressed on the surface of the same cell. These findings suggest that allelic exclusion of TcR genes in β transgenic mice depends on amount and/or onset of transgene expression during thymic development. Furthermore, TcR γ rearrangements and the population of TcR γ/δ‐bearing double‐negative CD4−CD8− thymocytes were reduced fivefold in type I transgenic animals. However, the Vγ usage and the γ/δ+ dendritic epidermal cell populations appeared normal. RNase protection analysis further revealed low levels of transgenic TcR β chain transcripts in TcR+ γ/δ CD4−CD8− thymocytes. These results suggest that the β transgene only quantitatively influences the γ/δ T cell compartment, and supports the independence of the γ/δ population. Copyright © 1990 Wiley‐VCH Verlag GmbH & Co. KGaA, Weinheim
Persistent Identifierhttp://hdl.handle.net/10722/292367
ISSN
2023 Impact Factor: 4.5
2023 SCImago Journal Rankings: 1.627
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorPircher, Hanspeter-
dc.contributor.authorOhashi, Pamela-
dc.contributor.authorMiescher, Guido-
dc.contributor.authorLang, Rosemarie-
dc.contributor.authorZikopoulos, Athanasios-
dc.contributor.authorBürki, Kurt-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorRobson MacDonald, H.-
dc.contributor.authorHengartner, Hans-
dc.date.accessioned2020-11-17T14:56:19Z-
dc.date.available2020-11-17T14:56:19Z-
dc.date.issued1990-
dc.identifier.citationEuropean Journal of Immunology, 1990, v. 20, n. 2, p. 417-424-
dc.identifier.issn0014-2980-
dc.identifier.urihttp://hdl.handle.net/10722/292367-
dc.description.abstractTo study allelic exclusion of TcR genes we analyzed two types (I and II) of TcR β transgenic mice. T cells derived from both types of mice contained similar amounts of transgenic RNA transcripts; however, surface expression of the transgenic β chain was drastically reduced in type II compared to type I. In type I transgenic mice, productive rearrangements and expression of endogenous TcR β genes were suppressed whereas on T cells of type II mice, both transgenic and endogenous TcR β chains were expressed on the surface of the same cell. These findings suggest that allelic exclusion of TcR genes in β transgenic mice depends on amount and/or onset of transgene expression during thymic development. Furthermore, TcR γ rearrangements and the population of TcR γ/δ‐bearing double‐negative CD4−CD8− thymocytes were reduced fivefold in type I transgenic animals. However, the Vγ usage and the γ/δ+ dendritic epidermal cell populations appeared normal. RNase protection analysis further revealed low levels of transgenic TcR β chain transcripts in TcR+ γ/δ CD4−CD8− thymocytes. These results suggest that the β transgene only quantitatively influences the γ/δ T cell compartment, and supports the independence of the γ/δ population. Copyright © 1990 Wiley‐VCH Verlag GmbH & Co. KGaA, Weinheim-
dc.languageeng-
dc.relation.ispartofEuropean Journal of Immunology-
dc.titleT cell receptor (TcR) β chain transgenic mice: Studies on allelic exclusion and on the TcR<sup>+</sup> γ/δ population-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/eji.1830200227-
dc.identifier.pmid1968840-
dc.identifier.scopuseid_2-s2.0-0025058127-
dc.identifier.volume20-
dc.identifier.issue2-
dc.identifier.spage417-
dc.identifier.epage424-
dc.identifier.eissn1521-4141-
dc.identifier.isiWOS:A1990CV89000026-
dc.identifier.issnl0014-2980-

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