Enhanced development of CD4+ γδ T cells in the absence of Itk results in elevated IgE production

Qian Qi, Mingcan Xia, Jianfang Hu, Elizabeth Hicks, Archana Iyer, Na Xiong, Avery August

Research output: Contribution to journalArticlepeer-review

69 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)564-571
Number of pages8
JournalBlood
Volume114
Issue number3
DOIs
StatePublished - 2009
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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