Itk and Th2 responses: action but no reaction

Yoko Kosaka, Martin Felices, Leslie J. Berg

Research output: Contribution to journalReview articlepeer-review

27 Scopus citations


The Tec family tyrosine kinase, Itk, was initially characterized as a crucial component of T-cell receptor signaling pathways resulting in phospholipase C-γ1 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.

Original languageEnglish (US)
Pages (from-to)453-460
Number of pages8
JournalTrends in Immunology
Issue number10
StatePublished - Oct 2006

Bibliographical note

Funding Information:
We acknowledge the following sources of support: NIH grants AI37584, AI46564 and AI66118, and a grant from the Center for Disease Control, CI000101. These sources had no role in the preparation or submission of this article.


Dive into the research topics of 'Itk and Th2 responses: action but no reaction'. Together they form a unique fingerprint.

Cite this