Cutting edge: STAT6 Signaling in eosinophils is necessary for development of allergic airway inflammation
Journal of Immunology, ISSN: 1550-6606, Vol: 194, Issue: 6, Page: 2477-2481
2015
- 18Citations
- 1Usage
- 23Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations18
- Citation Indexes18
- 18
- CrossRef17
- Usage1
- Abstract Views1
- Captures23
- Readers23
- 23
Article Description
Eosinophils are critical cellular mediators in allergic asthma and inflammation; however, the signals that regulate their functions are unclear. The transcription factor STAT6 regulates Th2 cytokine responses, acting downstream of IL-4 and IL-13. We showed previously that eosinophil-derived IL-13 plays an important role in the recruitment of T cells to the lung and the subsequent development of allergic asthma. However, whether eosinophils respond to Th2 signals to control allergic airway inflammation is unclear. In this report, we show that STAT6 eosinophils are unable to induce the development of allergic lung inflammation, including recruitment of CD4 T cells, mucus production, and development of airways hyperresponsiveness. This is likely due to the reduced migration of STAT6 eosinophils to the lung and in response to eotaxin. These data indicate that, like Th cells, eosinophils need to respond to Th2 cytokines via STAT6 during the development of allergic airway inflammation.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84924567190&origin=inward; http://dx.doi.org/10.4049/jimmunol.1402096; http://www.ncbi.nlm.nih.gov/pubmed/25681342; https://journals.aai.org/jimmunol/article/194/6/2477/104782/Cutting-Edge-STAT6-Signaling-in-Eosinophils-Is; https://digitalcommons.lsu.edu/vetmed_pubs/384; https://digitalcommons.lsu.edu/cgi/viewcontent.cgi?article=1384&context=vetmed_pubs; https://dx.doi.org/10.4049/jimmunol.1402096; http://www.jimmunol.org/content/194/6/2477; http://www.jimmunol.org/content/194/6/2477.abstract; http://www.jimmunol.org/content/194/6/2477.full.pdf; https://www.jimmunol.org/content/194/6/2477; https://www.jimmunol.org/content/194/6/2477.abstract; https://www.jimmunol.org/content/jimmunol/194/6/2477.full.pdf; http://www.jimmunol.org/cgi/doi/10.4049/jimmunol.1402096; http://www.jimmunol.org/lookup/doi/10.4049/jimmunol.1402096
Oxford University Press (OUP)
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