Abstract
Expression of T1ST2, the IL-33R, by Th2 cells requires GATA3. Resting Th2 cells express little GATA3, which is increased by IL-33 and a STAT5 activator, in turn increasing T1ST2 from its low-level expression on resting Th2 cells. Th2 cells that have upregulated T1ST2 produce IL-13, but not IL-4, in response to IL-33 plus a STAT5 activator in an antigen-independent, NF-kappaB-dependent, cyclosporin A (CsA)-resistant manner. Similarly, Th17 cells produce IL-17A in response to IL-1beta and a STAT3 activator and Th1 cells produce IFNgamma in response to IL-18 and a STAT4 inducer. Thus, each effector Th cell produces cytokines without antigenic stimulation in response to an IL-1 family member and a specific STAT activator, implying an innate mechanism through which memory CD4 T cells are recruited by an induced cytokine environment.
Publication types
-
Research Support, N.I.H., Intramural
MeSH terms
-
Animals
-
Cells, Cultured
-
Cytokines / biosynthesis*
-
GATA3 Transcription Factor / metabolism
-
Interleukin-1 / metabolism*
-
Interleukin-13 / metabolism
-
Interleukin-17 / metabolism
-
Interleukin-2 / biosynthesis
-
Interleukin-33
-
Interleukin-4 / metabolism
-
Interleukins / metabolism
-
Mice
-
NF-kappa B / metabolism
-
NFATC Transcription Factors / metabolism
-
Phosphorylation
-
Receptors, Antigen, T-Cell / metabolism
-
Receptors, Interleukin-1 / metabolism
-
STAT Transcription Factors / metabolism*
-
STAT5 Transcription Factor / metabolism
-
Th1 Cells / metabolism*
-
Th2 Cells / metabolism*
-
Up-Regulation
-
p38 Mitogen-Activated Protein Kinases / metabolism
Substances
-
Cytokines
-
GATA3 Transcription Factor
-
Il33 protein, mouse
-
Interleukin-1
-
Interleukin-13
-
Interleukin-17
-
Interleukin-2
-
Interleukin-33
-
Interleukins
-
NF-kappa B
-
NFATC Transcription Factors
-
Receptors, Antigen, T-Cell
-
Receptors, Interleukin-1
-
STAT Transcription Factors
-
STAT5 Transcription Factor
-
Interleukin-4
-
p38 Mitogen-Activated Protein Kinases