The Tec kinase Itk is critical for the development of αβ 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 γδ T cells in the thymus and spleen. This includes elevated numbers of CD4 + γδ T cell, the majority of which carry the Vγ1.1 and Vδ6.2/3 γδ T-cell receptor with a distinct phenotype. The development of these CD4 +γδ 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 + γδ 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 γδ 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 + γδ T cells in the absence of Itk. © 2009 by The American Society of Hematology.
Qi, Q., Xia, M., Hu, J., Hicks, E., Iyer, A., Xiong, N., & August, A. (2009). Enhanced development of CD4 + γδ T cells in the absence of Itk results in elevated IgE production. Blood, 114(3), 564–571. https://doi.org/10.1182/blood-2008-12-196345