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Antagonism of microRNA-126 suppresses the effector function of TH2 cells and the development of allergic airways disease.

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Title: Antagonism of microRNA-126 suppresses the effector function of TH2 cells and the development of allergic airways disease.
Authors: Mattes, Joerg1,2 joerg.mattes@newcastle.edu.au, Collison, Adam1,3, Plank, Maximilian1,3, Phipps, Simon3, Foster, Paul S.3 paul.foster@newcastle.edu.au
Source: Proceedings of the National Academy of Sciences of the United States of America. 11/3/2009, Vol. 106 Issue 44, p18704-18709. 6p. 4 Graphs.
Subjects: Asthma, House dust mites, Th2 cells, Antigens, RNA, Natural immunity, Transcription factors
Abstract: Allergic asthma is an inflammatory disease of the lung characterized by abnormal T helper-2 (TH2) lymphocyte responses to inhaled antigens. The molecular mechanisms leading to the generation of TH2 responses remain unclear, although toll-like receptors (TLRs) present on innate immune cells play a pivotal role in sensing molecular patterns and in programming adaptive T cell responses. Here we show that in vivo activation of TLR4 by house dust mite antigens leads to the induction of allergic disease, a process that is associated with expression of a unique subset of small, noncoding microRNAs. Selective blockade of microRNA (miR)-126 suppressed the asthmatic phenotype, resulting in diminished TH2 responses, inflammation, airways hyperresponsiveness, eosinophil recruitment, and mucus hypersecretion. miR-126 blockade resulted in augmented expression of POU domain class 2 associating factor 1, which activates the transcription factor PU.1 that alters TH2 cell function via negative regulation of GATA3 expression. In summary, this study presents a functional connection between miRNA expression and asthma pathogenesis, and our data suggest that targeting miRNA in the airways may lead to anti-inflammatory treatments for allergic asthma. [ABSTRACT FROM AUTHOR]
Copyright of Proceedings of the National Academy of Sciences of the United States of America is the property of National Academy of Sciences and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Engineering Source
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DbLabel: Engineering Source
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PubType: Academic Journal
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  Data: Antagonism of microRNA-126 suppresses the effector function of T<subscript>H</subscript>2 cells and the development of allergic airways disease.
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  Data: <searchLink fieldCode="AR" term="%22Mattes%2C+Joerg%22">Mattes, Joerg</searchLink><relatesTo>1,2</relatesTo><i> joerg.mattes@newcastle.edu.au</i><br /><searchLink fieldCode="AR" term="%22Collison%2C+Adam%22">Collison, Adam</searchLink><relatesTo>1,3</relatesTo><br /><searchLink fieldCode="AR" term="%22Plank%2C+Maximilian%22">Plank, Maximilian</searchLink><relatesTo>1,3</relatesTo><br /><searchLink fieldCode="AR" term="%22Phipps%2C+Simon%22">Phipps, Simon</searchLink><relatesTo>3</relatesTo><br /><searchLink fieldCode="AR" term="%22Foster%2C+Paul+S%2E%22">Foster, Paul S.</searchLink><relatesTo>3</relatesTo><i> paul.foster@newcastle.edu.au</i>
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  Data: <searchLink fieldCode="DE" term="%22Asthma%22">Asthma</searchLink><br /><searchLink fieldCode="DE" term="%22House+dust+mites%22">House dust mites</searchLink><br /><searchLink fieldCode="DE" term="%22Th2+cells%22">Th2 cells</searchLink><br /><searchLink fieldCode="DE" term="%22Antigens%22">Antigens</searchLink><br /><searchLink fieldCode="DE" term="%22RNA%22">RNA</searchLink><br /><searchLink fieldCode="DE" term="%22Natural+immunity%22">Natural immunity</searchLink><br /><searchLink fieldCode="DE" term="%22Transcription+factors%22">Transcription factors</searchLink>
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  Data: Allergic asthma is an inflammatory disease of the lung characterized by abnormal T helper-2 (TH2) lymphocyte responses to inhaled antigens. The molecular mechanisms leading to the generation of TH2 responses remain unclear, although toll-like receptors (TLRs) present on innate immune cells play a pivotal role in sensing molecular patterns and in programming adaptive T cell responses. Here we show that in vivo activation of TLR4 by house dust mite antigens leads to the induction of allergic disease, a process that is associated with expression of a unique subset of small, noncoding microRNAs. Selective blockade of microRNA (miR)-126 suppressed the asthmatic phenotype, resulting in diminished TH2 responses, inflammation, airways hyperresponsiveness, eosinophil recruitment, and mucus hypersecretion. miR-126 blockade resulted in augmented expression of POU domain class 2 associating factor 1, which activates the transcription factor PU.1 that alters TH2 cell function via negative regulation of GATA3 expression. In summary, this study presents a functional connection between miRNA expression and asthma pathogenesis, and our data suggest that targeting miRNA in the airways may lead to anti-inflammatory treatments for allergic asthma. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Proceedings of the National Academy of Sciences of the United States of America is the property of National Academy of Sciences and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1073/pnas.0905063106
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              Text: 11/3/2009
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