Submitted December 23, 2008
Accepted May 7, 2009
Enhanced development of CD4+ 
T cells in the absence of Itk results in elevated IgE production
Qian Qi, Mingcan Xia, Jianfang Hu, Elizabeth Hicks, Archana Iyer, Na Xiong, and Avery August*
Center for Molecular Immunology & Infectious Disease, and Department of Veterinary & Biomedical Sciences, The Pennsylvania State University, University Park, PA, United States
Immunology & Infectious Disease Graduate Program, The Pennsylvania State University, University Park, PA, United States
Schreyer's Honors College, The Pennsylvania State University, University Park, PA, United States
* Corresponding author; email: avery{at}psu.edu.
The Tec kinase Itk is critical for the development of 
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 MHC 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 WT 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.
