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dc.contributor.authorMiller, Andrew Todd
dc.contributor.authorBerg, Leslie J.
dc.date2022-08-11T08:09:02.000
dc.date.accessioned2022-08-23T16:15:56Z
dc.date.available2022-08-23T16:15:56Z
dc.date.issued2002-02-23
dc.date.submitted2008-11-21
dc.identifier.citation<p>J Immunol. 2002 Mar 1;168(5):2163-72.</p>
dc.identifier.issn0022-1767 (Print)
dc.identifier.doi10.4049/jimmunol.168.5.2163
dc.identifier.pmid11859102
dc.identifier.urihttp://hdl.handle.net/20.500.14038/34210
dc.description.abstractThe Tec family tyrosine kinase, IL-2-inducible T cell kinase (Itk), plays an important role in TCR signaling. Studies of T cells from Itk-deficient mice have demonstrated that Itk is critical for the activation of phospholipase-Cgamma1, leading to calcium mobilization in response to TCR stimulation. This biochemical defect results in reduced IL-2 production by Itk-deficient T cells. To further characterize the downstream effects of the Itk deficiency, we crossed Itk-/- mice to a TCR-transgenic line and examined T cell responses to stimulation by peptide plus APC. These studies show that Itk is required for maximal activation of early growth responses 2 and 3 and Fas ligand transcription after TCR stimulation. These transcriptional defects lead to reduced activation-induced cell death of stimulated Itk-/- T cells, both in vitro and in vivo. Together these studies define an important role for Itk in TCR signaling, leading to cytokine gene expression and activation-induced cell death.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11859102&dopt=Abstract">Link to article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.4049/jimmunol.168.5.2163
dc.subjectAnimals; *Apoptosis; CD4-Positive T-Lymphocytes; Calcium; Cells, Cultured; Cytochrome c Group; Fas Ligand Protein; Genes, T-Cell Receptor; Interleukin-2; *Lymphocyte Activation; MAP Kinase Signaling System; Membrane Glycoproteins; Mice; Mice, Knockout; Mice, Transgenic; Mitogen-Activated Protein Kinases; Protein-Tyrosine Kinases; Receptors, Antigen, T-Cell; Transcription Factors; Transcription, Genetic; Up-Regulation
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleDefective Fas ligand expression and activation-induced cell death in the absence of IL-2-inducible T cell kinase
dc.typeJournal Article
dc.source.journaltitleJournal of immunology (Baltimore, Md. : 1950)
dc.source.volume168
dc.source.issue5
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/867
dc.identifier.contextkey670714
html.description.abstract<p>The Tec family tyrosine kinase, IL-2-inducible T cell kinase (Itk), plays an important role in TCR signaling. Studies of T cells from Itk-deficient mice have demonstrated that Itk is critical for the activation of phospholipase-Cgamma1, leading to calcium mobilization in response to TCR stimulation. This biochemical defect results in reduced IL-2 production by Itk-deficient T cells. To further characterize the downstream effects of the Itk deficiency, we crossed Itk-/- mice to a TCR-transgenic line and examined T cell responses to stimulation by peptide plus APC. These studies show that Itk is required for maximal activation of early growth responses 2 and 3 and Fas ligand transcription after TCR stimulation. These transcriptional defects lead to reduced activation-induced cell death of stimulated Itk-/- T cells, both in vitro and in vivo. Together these studies define an important role for Itk in TCR signaling, leading to cytokine gene expression and activation-induced cell death.</p>
dc.identifier.submissionpathgsbs_sp/867
dc.contributor.departmentDepartment of Pathology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages2163-72


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