The key regulators of adult T helper cell responses, STAT6 and T-bet, are established in early life in mice

Shawn Rose, Patricia Guevara, Sandra Farach, Becky Adkins

Research output: Contribution to journalArticlepeer-review

6 Scopus citations


Murine neonatal immunity is typically Th2 biased. This is characterized by high-level IL-4 production at all phases of the immune response and poor IFN-γ memory responses. The differential expression of Th1/Th2 cytokines by neonates and adults could arise if the critical regulators of Th differentiation and function, STAT6 and T-bet, operate differently during the neonatal period. To test this idea, the Th cell responses of wild-type, T-bet-deficient, or STAT6-deficient mice were compared in vitro and in vivo. The absence of these factors had similar qualitative effects on the development of effector function in neonates and adults, i.e., if a Th lineage was inhibited or enhanced in adult animals, a similar phenomenon was observed in neonates. However, there was a striking difference observed in the in vivo Th1 memory responses of STAT6-deficient mice initially immunized as neonates. Antigen-specific IFN-γ production was increased 50-100-fold in STAT6-deficient neonates, achieving levels similar to those of STAT6-deficient adults. These findings demonstrate that STAT6 and T-bet signals are central in shaping Th responses in wild-type neonates, as in adult mice, and that the master regulators of Th cell development and function are already firmly established in early life.

Original languageEnglish (US)
Pages (from-to)1241-1253
Number of pages13
JournalEuropean Journal of Immunology
Issue number5
StatePublished - May 2006
Externally publishedYes


  • Cellular differentiation
  • Development
  • Ontogeny
  • Th1/Th2
  • Transcription factors

ASJC Scopus subject areas

  • Immunology


Dive into the research topics of 'The key regulators of adult T helper cell responses, STAT6 and T-bet, are established in early life in mice'. Together they form a unique fingerprint.

Cite this