Itk and Th2 responses: action but no reaction
Biochemistry & Molecular Pharmacology
Graduate School of Biomedical Sciences; Department of Pathology
Medical Subject Headings
Animals; Cell Differentiation; Humans; Lymphocyte Activation; Protein-Tyrosine Kinases; Signal Transduction; Th2 Cells
Life Sciences | Medicine and Health Sciences
The Tec family tyrosine kinase, Itk, was initially characterized as a crucial component of T-cell receptor signaling pathways resulting in phospholipase C-gamma1 activation and actin polymerization. In 1999, a seminal report by Fowell, Locksley and colleagues demonstrated that, in CD4+ T cells, Itk-dependent signals are differentially required for T-helper (Th)2 versus Th1 differentiation and effector function. These findings launched a series of in vitro and in vivo studies addressing the molecular defects of Itk-/- CD4+ T cells, and the impaired immune responses of intact Itk-deficient mice. While demonstrating a bias against Th2 differentiation, overall these experiments have indicated that the most significant failing is an inability of Itk-/- CD4+ T cells to produce Th2 cytokines in a recall response, rather than an absolute defect in Th2 differentiation by T cells lacking Itk. In this review, we discuss the pathways by which Itk might impact the differentiation of Th cells.
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Citation: Trends Immunol. 2006 Oct;27(10):453-60. Epub 2006 Aug 22. Link to article on publisher's site
Trends in immunology
Kosaka, Yoko; Felices, Martin; and Berg, Leslie J., "Itk and Th2 responses: action but no reaction" (2006). GSBS Student Publications. 621.