The zinc finger transcription factor Th-POK regulates CD4 versus CD8 T-cell lineage commitment

Xiao He, Xi He, Vibhuti P. Dave, Yi Zhang, Xiang Hua, Emmanuelle Nicolas, Weihong Xu, Bruce A. Roe and Dietmar J. Kappes ()
Additional contact information
Xiao He: Fox Chase Cancer Center
Xi He: Fox Chase Cancer Center
Vibhuti P. Dave: Fox Chase Cancer Center
Yi Zhang: Fox Chase Cancer Center
Xiang Hua: Fox Chase Cancer Center
Emmanuelle Nicolas: Fox Chase Cancer Center
Weihong Xu: University of Oklahoma
Bruce A. Roe: University of Oklahoma
Dietmar J. Kappes: Fox Chase Cancer Center

Nature, 2005, vol. 433, issue 7028, 826-833

Abstract: Abstract Development of immature T-cell precursors (thymocytes) to either the CD4 helper or CD8 killer T-cell lineages correlates precisely with their T-cell receptor specificity for major histocompatibility complex class II or class I molecules, respectively, indicating that the process is carefully regulated. Although intensively studied owing to its importance in determining the composition of the mature T-cell compartment and as a general model of binary lineage decisions, the underlying molecular pathways remain obscure. We have previously reported a spontaneous mouse mutant (HD (helper deficient) mice) in which lineage commitment is specifically perturbed without affecting positive selection. Here we show that a point mutation in the zinc finger transcription factor Th-POK (T-helper-inducing POZ/Krüppel-like factor) is responsible for redirection of class-II-restricted thymocytes to the CD8 lineage in HD mice. Furthermore, we demonstrate that constitutive expression of this factor during thymic development leads to redirection of class-I-restricted thymocytes to the CD4 lineage, indicating that Th-POK is a master regulator of lineage commitment.

Date: 2005
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DOI: 10.1038/nature03338

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