UMass Chan AffiliationsDepartment of Pathology
Program in Immunology and Virology
Graduate School of Biomedical Sciences
KeywordsAnimals; Antigens, CD28; CD4-Positive T-Lymphocytes; Glycogen Synthase Kinase 3; Immunologic Memory; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; NF-kappa B; Phenotype; Phosphorylation; Protein-Serine-Threonine Kinases; Protein-Tyrosine Kinases; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-akt; Receptors, Antigen, T-Cell; Signal Transduction
Medicine and Health Sciences
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AbstractItk, a member of the Tec family of tyrosine kinases, is critical for TCR signaling, leading to the activation of phospholipase C gamma1. Early biochemical studies performed in tumor cell lines also implicated Itk in CD28 signaling. These data were complemented by functional studies on primary Itk-/- T cells that suggested a negative role for Itk in CD28 signaling. In this report, we describe a thorough analysis of CD28-mediated responses in T cells lacking Itk. Using purified naive CD4+ T cells from Itk-/- mice, we examine a range of responses dependent on CD28 costimulation. We also analyze Akt and glycogen synthase kinase-3beta phosphorylation in response to stimulation of CD28 alone. Overall, these experiments demonstrate that CD28 signaling, as well as CD28-mediated costimulation of TCR signaling, function efficiently in the absence of Itk. These findings indicate that Itk is not essential for CD28 signaling in primary naive CD4+ T cells.
J Immunol. 2005 Apr 15;174(8):4475-9.
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/34027