File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Thymocyte selection in Vav and IRF-1 gene-deficient mice

TitleThymocyte selection in Vav and IRF-1 gene-deficient mice
Authors
Issue Date1998
Citation
Immunological Reviews, 1998, v. 165, p. 149-166 How to Cite?
AbstractT cells undergo a defined program of phenotypic and genetic changes during differentiation within the thymus. These changes define commitment of T-cell receptor (TCR)γδ and TCRαβ cells and lineage differentiation into CD4+ T helper and CD8+ cytotoxic T cells. T-cell differentiation and selection in the thymus constitute a tightly co-ordinated multistep journey through a network that can be envisaged as a three-dimensional informational highway made up of stromal cells and extracellular matrix molecules. This intrathymic journey is controlled by information exchange, with thymocytes depending on two-way cellular interactions with thymic stromal cells in order to receive essential signals for maturation and selection. Genetic inactivation of surface receptors, signal transduction molecules, and transcription factors using homologous recombination has provided novel insight into the signaling cascades that relay surface receptor engagement to gene transcription and subsequent progression of the developmental program. In this review we discuss molecular mechanisms of T lymphocyte development in mice that harbour genetic mutations in the guanine nucleotide exchange factor Vav and the interferon regulatory transcription factor 1 (IRF-1). We also propose a novel model of T-cell selection based on TCRα chain-directed signals for allelic exclusion and TCRα-based selection for single receptor usage.
Persistent Identifierhttp://hdl.handle.net/10722/291439
ISSN
2023 Impact Factor: 7.5
2023 SCImago Journal Rankings: 3.554
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorPenninger, Josef M.-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:54:22Z-
dc.date.available2020-11-17T14:54:22Z-
dc.date.issued1998-
dc.identifier.citationImmunological Reviews, 1998, v. 165, p. 149-166-
dc.identifier.issn0105-2896-
dc.identifier.urihttp://hdl.handle.net/10722/291439-
dc.description.abstractT cells undergo a defined program of phenotypic and genetic changes during differentiation within the thymus. These changes define commitment of T-cell receptor (TCR)γδ and TCRαβ cells and lineage differentiation into CD4+ T helper and CD8+ cytotoxic T cells. T-cell differentiation and selection in the thymus constitute a tightly co-ordinated multistep journey through a network that can be envisaged as a three-dimensional informational highway made up of stromal cells and extracellular matrix molecules. This intrathymic journey is controlled by information exchange, with thymocytes depending on two-way cellular interactions with thymic stromal cells in order to receive essential signals for maturation and selection. Genetic inactivation of surface receptors, signal transduction molecules, and transcription factors using homologous recombination has provided novel insight into the signaling cascades that relay surface receptor engagement to gene transcription and subsequent progression of the developmental program. In this review we discuss molecular mechanisms of T lymphocyte development in mice that harbour genetic mutations in the guanine nucleotide exchange factor Vav and the interferon regulatory transcription factor 1 (IRF-1). We also propose a novel model of T-cell selection based on TCRα chain-directed signals for allelic exclusion and TCRα-based selection for single receptor usage.-
dc.languageeng-
dc.relation.ispartofImmunological Reviews-
dc.titleThymocyte selection in Vav and IRF-1 gene-deficient mice-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1600-065X.1998.tb01237.x-
dc.identifier.pmid9850859-
dc.identifier.scopuseid_2-s2.0-0031725322-
dc.identifier.volume165-
dc.identifier.spage149-
dc.identifier.epage166-
dc.identifier.isiWOS:000077188400013-
dc.identifier.issnl0105-2896-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats