Abstract
IL-4 is important in Th2 differentiation and in cell expansion. Stat6 is necessary and sufficient for both functions. Although Gata3 is critical for Th2 polarization, it is not sufficient to mediate IL-4-driven cell expansion. We report that growth factor independent-1 (Gfi-1), a Stat6-dependent transcriptional repressor, strikingly increases Th2 cell expansion by promoting proliferation and preventing apoptosis. Cells infected with a Gfi-1 retrovirus show striking enhancement of IL-2-induced Stat5 phosphorylation and repression of p27(Kip-1) expression, suggesting a potential mechanism for the Gfi-1 growth effect. The synergy of Gfi-1 and Gata3 provides a mechanism through which IL-4 could selectively promote Th2 cell expansion.
MeSH terms
-
Animals
-
Apoptosis
-
Cells, Cultured
-
Coculture Techniques
-
DNA-Binding Proteins / biosynthesis*
-
DNA-Binding Proteins / genetics
-
DNA-Binding Proteins / physiology*
-
GATA3 Transcription Factor
-
Genetic Vectors
-
Interleukin-4 / pharmacology*
-
Kinetics
-
Lymphocyte Activation*
-
Mice
-
Mice, Inbred BALB C
-
Mice, Knockout
-
Models, Immunological
-
RNA, Messenger / biosynthesis
-
Retroviridae / genetics
-
STAT6 Transcription Factor
-
Th2 Cells / cytology
-
Th2 Cells / immunology*
-
Trans-Activators / genetics
-
Trans-Activators / physiology
-
Transcription Factors*
Substances
-
DNA-Binding Proteins
-
GATA3 Transcription Factor
-
Gata3 protein, mouse
-
Gfi1 protein, mouse
-
RNA, Messenger
-
STAT6 Transcription Factor
-
Stat6 protein, mouse
-
Trans-Activators
-
Transcription Factors
-
Interleukin-4