Transcriptional control of the IL-5 gene by human helper T cells: IL-5 synthesis is regulated independently from IL-2 or IL-4 synthesis

Mori, Akio; Kaminuma, Osamu; Mikami, Tadashi; Inoue, Satoshi; Okumura, Yasushi; Akiyama, Kazuo; Okudaira, Hirokazu

doi:10.1016/s0091-6749(99)70158-2

Cited by 44 publications

(29 citation statements)

References 44 publications

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“…Consistent with these observations, NF-κB levels in nuclear protein extracts from lung tissues were substantially increased in the OVA-induced model of allergic airway disease used for the present study. It is known that activation of this transcription factor induces a variety of inflammatory genes that are abnormally expressed in asthma (Barnes and Adcock, 1997;Mori et al, 1999;Stutz and Woisetschlager, 1999). We have also assessed whether these inflammatory cytokines are upregulated in the OVA-induced model of allergic airway disease.…”

Section: Discussionmentioning

confidence: 99%

A novel thiol compound, N-acetylcysteine amide, attenuates allergic airway disease by regulating activation of NF-κB and hypoxia-inducible factor-1α

Lee

Kim²,

Park³

et al. 2007

Exp Mol Med

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Reactive oxygen species (ROS) play an important role in the pathogenesis of airway inflammation and hyperresponsiveness. Recent studies have demonstrated that antioxidants are able to reduce airway inflammation and hyperreactivity in animal models of allergic airway disease. A newly developed antioxidant, small molecular weight thiol compound, N-acetylcysteine amide (AD4) has been shown to increase cellular levels of glutathione and to attenuate oxidative stress related disorders such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis. However, the effects of AD4 on allergic airway disease such as asthma are unknown. We used ovalbumin (OVA)-inhaled mice to evaluate the role of AD4 in allergic airway disease. In this study with OVA-inhaled mice, the increased ROS generation, the increased levels of Th2 cytokines and VEGF, the increased vascular permeability, the increased mucus production, and the increased airway resistance in the lungs were significantly reduced by the administration of AD4. We also found that the administration of AD4 decreased the increases of the NF-κB and hypoxia-inducible factor-1α (HIF-1α ) levels in nuclear protein extracts of lung tissues after OVA inhalation. These results suggest that AD4 attenuates airway inflammation and hyperresponsiveness by regulating activation of NF-κB and HIF-1α as well as reducing ROS generation in allergic airway disease.

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Section: Discussionmentioning

confidence: 99%

A novel thiol compound, N-acetylcysteine amide, attenuates allergic airway disease by regulating activation of NF-κB and hypoxia-inducible factor-1α

Lee

Kim²,

Park³

et al. 2007

Exp Mol Med

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“…The cytokines IL-2, IFN-␥, IL-5, and IL-10, all up-regulated by IMiDs, have all been found to be transcriptionally controlled by the transcription factor AP-1 (Jain et al, 1992;Sweetser et al, 1998;Mori et al, 1999;Gollnick et al, 2001). On the IL-2 promoter there are two AP-1 binding sites: the distal AP-1 site (position Ϫ179 to Ϫ185) and the proximal AP-1 site (position Ϫ145 to Ϫ152) (Hughes and Pober, 1996).…”

Section: Imids Increase Ap-1 Activity 1225mentioning

confidence: 99%

Enhancement of Cytokine Production and AP-1 Transcriptional Activity in T Cells by Thalidomide-Related Immunomodulatory Drugs

Schäfer¹,

Gandhi²,

Loveland³

et al. 2003

J Pharmacol Exp Ther

162

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“…Cooperative and coordinated recruitment of both nuclear factor of activated T cells and AP-1 is required for inducible transcription of IL-4 during T-cell activation (34,35). Although the genes for IL-4, IL-5, and IL-13 are closely located on human chromosome 5q31 (mouse chromosome 11) (36), there is evidence for the unique transcriptional regulation of IL-5 and IL-13 that is independent of AP-1 binding (37,38). Based on this information, one would predict that PNRI-299 should decrease IL-4 but not IL-5 or IL-13 expression.…”

Section: Identification Of Redox Effectormentioning

confidence: 99%

Chemogenomic identification of Ref-1/AP-1 as a therapeutic target for asthma

Nguyen

Teo

Matsuda

et al. 2003

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

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Asthma is characterized by an oxidant͞antioxidant imbalance in the lungs leading to activation of redox-sensitive transcription factors, nuclear factor B (NF-B), and activator protein-1 (AP-1). To develop therapeutic strategies for asthma, we used a chemogenomics approach to screen for small molecule inhibitor(s) of AP-1 transcription. We developed a ␤-strand mimetic template that acts as a reversible inhibitor (pseudosubstrate) of redox proteins. This template incorporates an enedione moiety to trap reactive cysteine nucleophiles in the active sites of redox proteins. Specificity for individual redox factors was achieved through variations in X and Y functionality by using a combinatorial library approach. A limited array (2 ؋ 6) was constructed where X was either NHCH 3

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Transcriptional control of the IL-5 gene by human helper T cells: IL-5 synthesis is regulated independently from IL-2 or IL-4 synthesis

Cited by 44 publications

References 44 publications

A novel thiol compound, N-acetylcysteine amide, attenuates allergic airway disease by regulating activation of NF-κB and hypoxia-inducible factor-1α

A novel thiol compound, N-acetylcysteine amide, attenuates allergic airway disease by regulating activation of NF-κB and hypoxia-inducible factor-1α

Enhancement of Cytokine Production and AP-1 Transcriptional Activity in T Cells by Thalidomide-Related Immunomodulatory Drugs

Chemogenomic identification of Ref-1/AP-1 as a therapeutic target for asthma

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