Differentiation of T-helper lymphocytes: Selective regulation by members of the STAT family of transcription factors

Ulrike Schindler, Timothy Hoey, Steven L. McKnight

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

Interleukin-4 (IL-4) and interleukin-12 (IL-12) control the differentiation of T-helper cells. Here we summarize studies which investigate the mechanism by which these cytokines selectively reprogramme gene expression in T-lymphocytes. Cytokine stimulation leads to the phosphorylation of specific tyrosine residues within the intracellular domain of the corresponding cytokine receptor. These phosphotyrosines serve as docking sites for latent, cytoplasmic transcription factors known as signal transducers and activators of transcription (Stat) proteins. Receptor/Stat interaction is mediated by the src homology 2 (SH2) domain of the corresponding Stat protein. Although Stat binding to the intracellular domain of the cytokine receptor strongly depends on the phosphotyrosine residue, the recruitment of a specific Stat protein is dictated by amino acid residues C-terminal to the phosphotyrosine. Specific docking sites within individual cytokine receptors have been identified for almost all Stat proteins. The direct coupling between cytokine receptor and transcription factor helps to explain how different cytokines elicit distinct patterns of gene expression.

Original languageEnglish (US)
Pages (from-to)507-515
Number of pages9
JournalGenes to Cells
Volume1
Issue number6
DOIs
StatePublished - Jan 1 1996

ASJC Scopus subject areas

  • Genetics
  • Cell Biology

Fingerprint Dive into the research topics of 'Differentiation of T-helper lymphocytes: Selective regulation by members of the STAT family of transcription factors'. Together they form a unique fingerprint.

  • Cite this