Gene expression of the GATA-3 transcription factor is increased in atopic asthma

Nakamura, Yutaka; Ghaffar, Omar; Olivenstein, Ronald; Taha, Rame; Gounni, Abdelilah Soussi; Zhang, Dong-Hong; Ray, Anuradha; Hamid, Qutayba

doi:10.1016/s0091-6749(99)70493-8

Cited by 186 publications

(137 citation statements)

References 46 publications

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“…Th1 cells produce IFN-␥, IL-9, IL-13, granulocyte-macrophage colony-stimulating factor, and chemokines in response to Ag, IL-2, and IL-18 in vitro (22,25). Among the cytokines produced, IL-13 is most bronchogenic and participates in AHR (7)(8)(9)(10)(11)(12)(13). However, neutralization of IL-13 in the lungs fails to inhibit Th1-cell-induced AHR (22).…”

Section: Resultsmentioning

confidence: 99%

“…Histologically, there are infiltrates of eosinophils, degranulated mast cells, subbasement membrane thickening, hyperplasia and hypertrophy of bronchial smooth muscle, and hyperplasia of airway goblet cells (1,2). Th2 cells have been recognized as inducing bronchial asthma by production of Th2 cytokines (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12). Particularly, IL-13 is suggested to play a critical role in induction of AHR, eosinophilic infiltration, goblet cell metaplasia, and lung fibrosis (9)(10)(11)(12)(13).…”

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confidence: 99%

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T helper 1 cells stimulated with ovalbumin and IL-18 induce airway hyperresponsiveness and lung fibrosis by IFN-γ and IL-13 production

Hayashi¹,

Yoshimoto²,

Izuhara

et al. 2007

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

124

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We previously reported that ovalbumin (OVA) and IL-18 nasally administered act on memory type T helper (Th)1 cells to induce airway hyperresponsiveness (AHR) and inflammation, which is characterized by peribronchial infiltration with neutrophils and eosinophils. Here, we report this administration also induces lung fibrosis in an IL-13-dependent manner. bronchial asthma ͉ LPS ͉ periostin ͉ hydroxy proline ͉ airway inflammation

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

T helper 1 cells stimulated with ovalbumin and IL-18 induce airway hyperresponsiveness and lung fibrosis by IFN-γ and IL-13 production

Hayashi¹,

Yoshimoto²,

Izuhara

et al. 2007

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

124

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“…On the other hand, the Th2-induced transcription factor GATA-3 specifically controls the expression of Th2 cytokines, which are essential to induce allergic inflammation in vivo (Zheng & Flavell 1997). In fact, increased levels of GATA-3 mRNA expression have been reported in asthmatic airways when compared to those of control subjects and correlated with increased IL-5 expression (Nakamura et al 1999). The expression of a dominant-negative mutant of GATA-3 led to a reduction in the levels of all Th2 cytokines and attenuated mucus production, IgE synthesis, and airway eosinophilia in the transgenic mice .…”

Section: Ifn-γ γ γ γ γ and Th Immune Responsementioning

confidence: 99%

The role of interferon-gamma on immune and allergic responses

Teixeira

Fonseca

Barboza

et al. 2005

Mem. Inst. Oswaldo Cruz

109

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“…Interestingly, haplotype analysis of the GATA3 locus showed associations with asthma and atopy-related phenotypes (25). 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: 99%

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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Gene expression of the GATA-3 transcription factor is increased in atopic asthma

Cited by 186 publications

References 46 publications

T helper 1 cells stimulated with ovalbumin and IL-18 induce airway hyperresponsiveness and lung fibrosis by IFN-γ and IL-13 production

T helper 1 cells stimulated with ovalbumin and IL-18 induce airway hyperresponsiveness and lung fibrosis by IFN-γ and IL-13 production

The role of interferon-gamma on immune and allergic responses

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

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