Upregulation of the transcription factor GATA-3 in upper airway mucosa after in vivo and in vitro allergen challenge

Nakamura, Yutaka; Christodoulopoulos, Pota; Cameron, Lisa; Wright, Erin D.; Lavigne, François; Toda, Masao; Muro, Shigeo; Ray, Anuradha; Eidelman, David H.; Minshall, Eleanor; Hamid, Qutayba

doi:10.1067/mai.2000.107045

Cited by 52 publications

(41 citation statements)

References 25 publications

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“…ZHANG et al [40] created transgenic mice expressing an inducible GATA3 dominant negative in T-cells, and provided definitive evidence of the role of GATA3 in allergen-driven Th2 cytokine production and airway inflammation. Studies analysing GATA3 expression by immunohistochemistry found that GATA3 expressing cells were more numerous in airway biopsies from asthmatic compared with control subjects, and that GATA3-positive cells were strikingly increased following allergen challenge [29,221]. If GATA3 expression is used as a surrogate marker of Th2 commitment, then these studies show that there is a striking enrichment of…”

Section: Gata3mentioning

confidence: 89%

T-helper cell type-2 regulation in allergic disease

et al. 2005

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Substantial experimental evidence now supports the notion that allergic diseases are characterised by a skewing of the immune system towards a T-helper cell type-2 (Th2) phenotype.Studies using both human and mouse model systems have provided key evidence for the role that Th2 cytokines play in driving many of the hallmarks of allergic inflammation. Furthermore, the signalling pathways by which Th2 cytokines exert their effects on airway target cells are rapidly being elucidated, and antagonists of the Th2 pathway are under active development.In this review, the current knowledge of the role of T-helper cell type-2 cells in asthma is summarised, focusing on how and where T-helper cell type-2 cells differentiate from naïve precursors. The signalling molecules and transcription factors involved in T-helper cell type-2 differentiation will be reviewed in detail, in an attempt to translate studies using genetically modified mice into meaningful insights about asthma and other allergic diseases.

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Section: Gata3mentioning

confidence: 89%

T-helper cell type-2 regulation in allergic disease

et al. 2005

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“…Nakamura et al (26) showed that GATA3 expression is increased in lung mucosa and bronchoalveolar lavage (BAL) cells of asthmatic patients, compared with healthy control subjects. Moreover, Gata3 expression was increased after local allergen provocation, in the absence of inflammatory cell recruitment (27).…”

mentioning

confidence: 98%

Enforced Expression of Gata3 in T Cells and Group 2 Innate Lymphoid Cells Increases Susceptibility to Allergic Airway Inflammation in Mice

KleinJan

Wolterink

Levani

et al. 2014

The Journal of Immunology

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Airway inflammation in allergic asthma reflects a threshold response of the innate immune system, including group 2 innate lymphoid cells (ILC2), followed by an adaptive Th2 cell–mediated response. Transcription factor Gata3 is essential for differentiation of both Th2 cells and ILC2. We investigated the effects of enforced Gata3 expression in T cells and ILC2 on the susceptibility of mice to allergic airway inflammation (AAI). We used CD2-Gata3 transgenic (Tg) mice with enforced Gata3 expression driven by the CD2 promoter, which is active both in T cells and during ILC2 development. CD2-Gata3 Tg mice and wild-type (WT) littermates were analyzed in mild models of AAI without adjuvants. Whereas OVA allergen exposure did not induce inflammation in WT controls, CD2-Gata3 Tg mice showed clear AAI and enhanced levels of IL-5 and IL-13 in bronchoalveolar lavage. Likewise, in house dust mite–driven asthma, CD2-Gata3 Tg mice were significantly more susceptible to AAI than WT littermates, whereby both ILC2 and Th2 cells were important cellular sources of IL-5 and IL-13 in bronchoalveolar lavage and lung tissue. Compared with WT littermates, CD2-Gata3 Tg mice contained increased numbers of ILC2, which expressed high levels of IL-33R and contributed significantly to early production of IL-4, IL-5, and IL-13. CD2-Gata3 Tg mice also had a unique population of IL-33–responsive non-B/non-T lymphoid cells expressing IFN-γ. Enforced Gata3 expression is therefore sufficient to enhance Th2 and ILC2 activity, and leads to increased susceptibility to AAI after mild exposure to inhaled harmless Ags that otherwise induce Ag tolerance.

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“…One line of study demonstrated that GATA-3 expression is increased within the bronchial mucosa of allergic asthmatic patients and the nasal mucosa of allergic rhinitis patients. 18,19) In addition, ectopic expression of dominantnegative mutants of GATA-3 successively inhibits the allergic inflammation in a murine model of asthma. 20) However, SCRT suppresses Th2 cell development by regulating factors other than GATA-3, since SCRT does not directly affect GATA-3 expression (Fig.…”

Section: Discussionmentioning

confidence: 99%

So-Cheong-Ryong-Tang, Tradititional Korean Medicine, Suppresses Th2 Lineage Development

Rho

Cho

et al. 2004

Biological & Pharmaceutical Bulletin

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The present study was designed to evaluate the effect of So-Cheong-Ryong-Tang (SCRT, also called ShoSeiryu-To or Xiao-Qing-Long-Tang) on helper T cell development by monitoring Th1/Th2-specific cytokine secretion patterns in artificially induced Th1 or Th2 polarized conditions. The results demonstrated that Th2 cells were dramatically underpopulated in the Th2-driven condition triggered by SCRT treatment, while the Th1 cells were not altered in the Th1-skewed condition. Furthermore, under Th2-skewed conditions the levels of interleukin-4 were considerably decreased with SCRT treatment. The expression of GATA-3, a transcription factor that plays a pivotal role in Th2 lineage programming, did not change with SCRT treatment, while the expression of another Th2 transcription factor, c-Maf, was dramatically suppressed. These data suggest that SCRT modulates Th2 development by suppressing c-Maf expression. This study implies that the SCRT effect on CD4؉ T cells is a key pharmacologic point of effect for treating IgE-mediated allergic asthma. These results also suggest that SCRT might be a useful agent for the correction of Th2-dominant pathologic disorders.

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Upregulation of the transcription factor GATA-3 in upper airway mucosa after in vivo and in vitro allergen challenge

Cited by 52 publications

References 25 publications

T-helper cell type-2 regulation in allergic disease

T-helper cell type-2 regulation in allergic disease

Enforced Expression of Gata3 in T Cells and Group 2 Innate Lymphoid Cells Increases Susceptibility to Allergic Airway Inflammation in Mice

So-Cheong-Ryong-Tang, Tradititional Korean Medicine, Suppresses Th2 Lineage Development

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