Correlation between the ratio of T-bet/GATA-3 and the levels of IL-4 and IFN-γ in patients with allergic asthma

Ji, Yong; Chen, Guoqiang; Huang, Bin; Wu, Song

doi:10.3892/mmr.2011.469

Cited by 11 publications

(8 citation statements)

References 16 publications

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“…Since naïve CD4 + T cells from SMAR1 −/− mice have impaired Th2 differentiation in the lung, allergic inflammation leads to aberrant expression of genes that are responsible for Th1 and Th17 commitment, which in turn suppresses Th2 response in vivo . This observation is in line with the previous reports suggesting the elevated T-bet expression in SMAR1 −/− mice after chronic allergic antigen exposure ( 41 , 71 , 73 ). It shows SMAR1 is a novel and essential factor for the establishment of Th2 cells by functioning as a Th1-specific transcriptional gene repressor.…”

Section: Nuclear Matrix-binding Protein Smar1: Essential Regulator Ofsupporting

confidence: 93%

Chromatin Remodeling Protein SMAR1 Is a Critical Regulator of T Helper Cell Differentiation and Inflammatory Diseases

2017

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T cell differentiation from naïve T cells to specialized effector subsets of mature cells is determined by the iterative action of transcription factors. At each stage of specific T cell lineage differentiation, transcription factor interacts not only with nuclear proteins such as histone and histone modifiers but also with other factors that are bound to the chromatin and play a critical role in gene expression. In this review, we focus on one of such nuclear protein known as tumor suppressor and scaffold matrix attachment region-binding protein 1 (SMAR1) in CD4+ T cell differentiation. SMAR1 facilitates Th1 differentiation by negatively regulating T-bet expression via recruiting HDAC1–SMRT complex to its gene promoter. In contrast, regulatory T (Treg) cell functions are dependent on inhibition of Th17-specific genes mainly IL-17 and STAT3 by SMAR1. Here, we discussed a critical role of chromatin remodeling protein SMAR1 in maintaining a fine-tuned balance between effector CD4+ T cells and Treg cells by influencing the transcription factors during allergic and autoimmune inflammatory diseases.

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Section: Nuclear Matrix-binding Protein Smar1: Essential Regulator Ofsupporting

confidence: 93%

Chromatin Remodeling Protein SMAR1 Is a Critical Regulator of T Helper Cell Differentiation and Inflammatory Diseases

2017

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“…A previous studied showed that the mRNA expression levels of T-bet and IFN-γ were lower, whereas the mRNA expression levels of GATA-3 and IL-4 were higher in the nasal mucosa of AR mice compared with those of normal mice, thus inhibiting the Th1 immune response and enhancing the Th2 immune response, respectively (40). The mRNA imbalance of T-bet/GATA-3 and IFN-γ/IL-4 results in an imbalance of the Thl/Th2 immune response (4,41), which leads to the occurrence of AR. Enhancing the Th1 and/or reducing the Th2 immune response to correct the Thl/Th2 imbalance may prevent allergic inflammatory reactions and ease the symptoms of allergic diseases (2–3,5,13–15).…”

Section: Discussionmentioning

confidence: 99%

Regulatory effect of microRNA-135a on the Th1/Th2 imbalance in a murine model of allergic rhinitis

Luo

Deng

Tao

et al. 2014

Experimental and Therapeutic Medicine

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Allergic rhinitis (AR) is primarily caused by a T helper cell (Th)1/Th2 imbalance. In a murine AR model of a previous study, the serum ovalbumin (OVA)-sIgE concentration was high, whereas microRNA (miR)-135a was lowly expressed in the nasal mucosa. The abnormal expression pattern of miR-135a coincided with highly expressed endogenous factors, including GATA binding protein (GATA)-3 and interleukin (IL)-4, and lowly expressed factors, including T-box expressed in T cells (T-bet) and interferon (IFN)-γ. We hypothesized that miR-135a may play an important role in immune regulation in AR mice. In the present study, AR was induced by OVA in the mice. Two groups of the AR mice were treated with a miR-135a mimic and a mimic control, respectively. The serum and nasal mucosa were collected for analysis. Following miR-135a application, the serum OVA-sIgE concentration was significantly reduced. In the nasal mucosa, the expression levels of miR-135a were higher, the mRNA and protein expression levels of GATA-3 and IL-4 were lower, and the expression levels of T-bet and IFN-γ were higher. The miR-135a corrected the Th1/Th2 imbalance in the AR mice. Findings of this study may provide a basis for novel genetic treatments in addressing allergic diseases.

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“…However, during the preclinical safety evaluation of drugs, allergic reaction is among the most difficult factors to predict due to the lack of appropriate models for predicting clinical allergic reactions (15). The establishment of appropriate animal models for allergic reaction prediction, and their successful application to predicting drug allergies are required (16,17). The present results demonstrated that Artemisia extract pretreatment is capable of reducing the systemic anaphylactic shock, histamine release, scratching behavior and vascular permeability induced by compound 48/80.…”

Section: Discussionmentioning

confidence: 65%

Anti-allergic effect of Artemisia extract in rats

Deng

Liu

Geng

2016

Experimental and Therapeutic Medicine

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Abstract. Artemisia apiacea (also known as Artemisia annua L) is a herb commonly used in traditional Chinese medicine. In the early 1970s, artemisinin was isolated and identified as the active antimalarial ingredient, and thereafter, A. apiacea and artemisinin have been studied extensively, such as anti-inflammation and antipyresis, antibacteria, antiparasitic and immunosuppression effects of A. apiacea extract. The present study investigated the extracts anti-allergic effect obtained from the dried flowering tips of A. apiacea in rats. A systemic anaphylactic reaction model was induced in rats using compound 48/80. Artemisia extract was administered 1 h prior to the injection of compound 48/80. Artemisia was extracted from dried flowering tips of A. deserti using 80% ethanol. Subsequently, the systemic anaphylactic shock, histamine release, scratching behavior and vascular permeability induced by compound 48/80 were evaluated. The administration of Artemisia extract at 200 and 400 mg/kg doses suppressed the systemic anaphylactic shock induced by compound 48/80 in a dose-dependent manner. Overall, the Artemisia extract was able to effectively decrease systemic anaphylactic shock, histamine release, scratching behavior and vascular permeability induced by compound 48/80 in a dose-dependent manner.

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Correlation between the ratio of T-bet/GATA-3 and the levels of IL-4 and IFN-γ in patients with allergic asthma

Cited by 11 publications

References 16 publications

Chromatin Remodeling Protein SMAR1 Is a Critical Regulator of T Helper Cell Differentiation and Inflammatory Diseases

Chromatin Remodeling Protein SMAR1 Is a Critical Regulator of T Helper Cell Differentiation and Inflammatory Diseases

Regulatory effect of microRNA-135a on the Th1/Th2 imbalance in a murine model of allergic rhinitis

Anti-allergic effect of Artemisia extract in rats

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