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Blood, 16 July 2009, Vol. 114, No. 3, pp. 564-571.
Prepublished online as a Blood First Edition Paper on May 14, 2009; DOI 10.1182/blood-2008-12-196345.
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IMMUNOBIOLOGY
Enhanced development of CD4+   T cells in the absence of Itk results in elevated IgE production
Qian Qi1,2,
Mingcan Xia1,2,
Jianfang Hu1,2,
Elizabeth Hicks1,3,
Archana Iyer1,2,
Na Xiong1, and
Avery August1
1 Center for Molecular Immunology & Infectious Disease and Department of Veterinary & Biomedical Sciences,
2 Immunology & Infectious Disease Graduate Program, and
3 Schreyer's Honors College, Pennsylvania State University, University Park
The Tec kinase Itk is critical for the development of  β T cells as well as differentiation of CD4+ T cells into Th2 cells. Itk null mice have defects in the production of Th2 cytokines; however, they paradoxically have significant elevations in serum IgE. Here we show that Itk null mice have increased numbers of   T cells in the thymus and spleen. This includes elevated numbers of CD4+ T cell, the majority of which carry the V1.1 and V6.2/3 T-cell receptor with a distinct phenotype. The development of these CD4+ T cells is T cell intrinsic, independent of either major histocompatibility complex class I or class II, and is favored during development in the absence of Itk. Itk null CD4+ T cells secrete significant amounts of Th2 cytokines and can induce the secretion of IgE by wild-type B cells. Our data indicate that Itk plays important role in regulating T-cell development and function. In addition, our data indicate that the elevated IgE observed in Itk-deficient mice is due in part to the enhanced development of CD4+ T cells in the absence of Itk.
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