6533b7ddfe1ef96bd1273f0c
RESEARCH PRODUCT
p38 MAP kinase drives the expression of mast cell-derived IL-9 via activation of the transcription factor GATA-1.
Matthias KleinValeska HeibTobias BoppMarc BeckerChristoph RichterStefan Klein-hesslingMichael StassenEdgar SchmittEdgar SerflingHansjörg SchildChristine Neudörflsubject
MaleCell signalingmedicine.medical_treatmentImmunologyBone Marrow CellsGATA3 Transcription FactorBiologyp38 Mitogen-Activated Protein KinasesTransactivationMiceTh2 CellsmedicineAnimalsGATA1 Transcription FactorMast CellsRNA MessengerPhosphorylationPromoter Regions GeneticMolecular BiologyInterleukin 5Mice Inbred BALB CGATA2Interleukin-9Mast cellCell biologyInterleukin 33GATA2 Transcription FactorCytokinemedicine.anatomical_structureGene Expression RegulationInterleukin 15MutationFemaledescription
Mast cells are able to produce a huge panel of mediators including the Th2-type cytokine IL-9, which is considered to be a key mediator for the pathogenesis of allergic asthma, but detailed information on the regulation of IL-9 transcription in mast cells has been scarce. Herein we provide evidence that the erythroid/myeloid transcription factor GATA-1, which is not expressed in Th2 cells, is a potent activator of IL-9 expression in murine bone marrow-derived mast cells (BMMC). Furthermore, in mast cells, but not in Th2 cells, production of IL-9 is sensitive to inhibition of p38 MAP kinase. As transactivation mediated by GATA-1 is also sensitive to inhibition of p38 MAP kinase, and GATA-1 is a target for p38 MAP kinase-mediated phosphorylation in vitro, we conclude that both signaling molecules represent a part of a mast cell-specific signaling network that regulates the expression of IL-9.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2007-02-01 | Molecular immunology |