GATA-3 Has Dual Regulatory Functions in Human Interleukin-5 Transcription

Schwenger, Gretchen G.T.F.; Fournier, Régis; Kok, Chee Choy; Mordvinov, Viatcheslav A.; Yeoman, Deborah; Sanderson, Colin C.J.

doi:10.1074/jbc.m107836200

Cited by 44 publications

(43 citation statements)

References 34 publications

(40 reference statements)

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“…25,42 However, IL-5 is the only cytokine which appears to be regulated by GATA-3 in human. 43 In mice, c-Maf has a critical and selective function in IL-4 gene transcription. 44 c-Maf mRNA has predominantly been observed in human and murine Th2 cells.…”

Section: Discussionmentioning

confidence: 99%

Expression of the T-Cell Transcription Factors, GATA-3 and T-bet, in the Neoplastic Cells of Hodgkin Lymphomas

Atayar

Poppema

Blokzijl

et al. 2005

The American Journal of Pathology

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Since Hodgkin and Reed-Sternberg (HRS) cells of Hodgkin lymphoma (HL) generally have immuno-1-4 Immunohistochemical analysis of the neoplastic cells of CHL has revealed an immunophenotype that is very specific, but highly unusual for a B-cell-derived tumor. The so-called Hodgkin and Reed-Sternberg (HRS) cells typically express CD30 and CD15, have inconsistent expression of CD20 and CD79a, and typically lack J-chain and immunoglobulins. 5,6 The neoplastic cells of NLPHL, the so-called lymphocytic and histiocytic (L&H)-type HRS cells, do express classical B-cell markers like CD20, CD79a, and J-chain 7 but lack CD30 and CD15.

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Section: Discussionmentioning

confidence: 99%

Expression of the T-Cell Transcription Factors, GATA-3 and T-bet, in the Neoplastic Cells of Hodgkin Lymphomas

Atayar

Poppema

Blokzijl

et al. 2005

The American Journal of Pathology

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“…Although GATA3 is reported to be a downstream target of NF-B activation (31) and is critical for chromatin remodeling of the Th2 cytokine gene loci (32)(33)(34) and transcription of the IL-5 and IL-13 genes in Th2 cells (35)(36)(37), GATA3 is not expressed in BMMCs (7). In contrast, GATA1 and -2 play a key role in mast-cell differentiation (38,39).…”

Section: Lps Treatment Induces Nf-b Activation and Increases Expressimentioning

confidence: 99%

Regulation of allergic airway inflammation through Toll-like receptor 4-mediated modification of mast cell function

Nigo¹,

Yamashita²,

Hirahara³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

136

135

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In a mouse experimental asthma model, the administration of bacterial lipopolysaccharide (LPS), particularly at low doses, enhances the levels of ovalbumin (OVA)-induced eosinophilic airway inflammation. In an effort to clarify the cellular and molecular basis for the LPS effect, we demonstrate that the OVA-induced eosinophilic inflammation in the lung is dramatically increased by the administration of LPS in wild-type mice, whereas such increase was not observed in mast-cell-deficient mice or Toll-like receptor (TLR)4-deficient mice. Adoptive transfer of bone-marrow-derived mast cells (BMMCs) from wild-type, but not from TLR4-deficient, mice restored the increased eosinophilic inflammation in mast-celldeficient mice. Wild-type BMMCs pretreated with LPS in vitro also reconstituted the eosinophilic inflammation. Moreover, in vitro analysis revealed that the treatment of BMMCs with LPS resulted in NF-B activation, sustained up-regulation of GATA1 and -2 expression, and increased the capability to produce IL-5 and -13. Dramatic increases in the expression of IL-5 and -13 and Eotaxin 2 were detected in LPS-treated BMMCs after costimulation with LPS and IgE͞Ag. Overexpression of GATA1, but not GATA2, in MC9 mast cells resulted in increased transcriptional activity of IL-4, -5, and -13. Furthermore, the levels of transcription of Th2 cytokines in BMMCs were decreased by the introduction of small interfering RNA for GATA1. Thus, mast cells appear to control allergic airway inflammation after their activation and modulation through TLR4-mediated induction of GATA1 and subsequent increase in Th2 cytokine production.cytokine ͉ GATA1 ͉ mast cell ͉ lipopolysaccharide ͉ bone-marrow-derived mast cells

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“…Ϫ/Ϫ Developing Th2 Cells-GATA3 has been reported to be a critical transcriptional factor for the suppression of IFN␥ production (38 -40) and the activation of IL-5 transcription (41)(42)(43). Therefore, we checked the expression of GATA3 in the Gfi1 Ϫ/Ϫ Th2 cells.…”

Section: Enhanced Ubiquitin/proteasome-dependent Degradation Of Gata3mentioning

confidence: 99%

Gfi1-mediated Stabilization of GATA3 Protein Is Required for Th2 Cell Differentiation

Shinnakasu

Yamashita

Kuwahara

et al. 2008

Journal of Biological Chemistry

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The differentiation of naive CD4 T cells into Th2 cells requires the T cell receptor-mediated activation of the ERK MAPK cascade. Little is known, however, in regard to how the ERK MAPK cascade regulates Th2 cell differentiation. We herein identified Gfi1 (growth factor independent-1) as a downstream target of the ERK MAPK cascade for Th2 cell differentiation. In the absence of Gfi1, interleukin-5 production and the change of histone modification at the interleukin-5 gene locus were severely impaired. Furthermore, the interferon ␥ gene showed a striking activation in the Gfi1 ؊/؊ Th2 cells. An enhanced ubiquitin/ proteasome-dependent degradation of GATA3 protein was observed in Gfi1 ؊/؊ Th2 cells, and the overexpression of GATA3 eliminated the defect of Th2 cell function in Gfi1-deficient Th2 cells. These data suggest that the T cell receptor-mediated induction of Gfi1 controls Th2 cell differentiation through the regulation of GATA3 protein stability.

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GATA-3 Has Dual Regulatory Functions in Human Interleukin-5 Transcription

Cited by 44 publications

References 34 publications

Expression of the T-Cell Transcription Factors, GATA-3 and T-bet, in the Neoplastic Cells of Hodgkin Lymphomas

Expression of the T-Cell Transcription Factors, GATA-3 and T-bet, in the Neoplastic Cells of Hodgkin Lymphomas

Regulation of allergic airway inflammation through Toll-like receptor 4-mediated modification of mast cell function

Gfi1-mediated Stabilization of GATA3 Protein Is Required for Th2 Cell Differentiation

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