Stat5 is required for IL-2-induced cell cycle progression of peripheral T cells

Richard Moriggl, David J. Topham, Stephan Teglund, Veronika Sexl, Catriona McKay, Demin Wang, Angelika Hoffmeyer, Jan Van Deursen, Mark Y. Sangster, Kevin D. Bunting, Gerard C. Grosveld, James N. Ihle

Research output: Contribution to journalArticlepeer-review

461 Scopus citations


Many cytokines activate two highly homologous Stat proteins, 5a and 5b. Mice deficient in both genes lack all growth hormone and prolactin functions but retain functions associated with cytokines such as erythropoietin. Here, we demonstrate that, while lymphoid development is normal, Stat5a/b mutant peripheral T cells are profoundly deficient in proliferation and fail to undergo cell cycle progression or to express genes controlling cell cycle progression. In addition, the mice lack NK cells, develop splenomegaly, and have T cells with an activated phenotype, phenotypes seen in IL-2 receptor β chain-deficient mice. These phenotypes are not seen in mice lacking Stat5a or Stat5b alone. The results demonstrate that the Stat5 proteins, redundantly, are essential mediators of IL-2 signaling in T cells.

Original languageEnglish (US)
Pages (from-to)249-259
Number of pages11
Issue number2
StatePublished - Feb 1999

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases


Dive into the research topics of 'Stat5 is required for IL-2-induced cell cycle progression of peripheral T cells'. Together they form a unique fingerprint.

Cite this