TY - JOUR
T1 - Cutting edge
T2 - STAT6 Signaling in eosinophils is necessary for development of allergic airway inflammation
AU - Stokes, Kindra
AU - LaMarche, Nelson M.
AU - Islam, Nasif
AU - Wood, Amie
AU - Huang, Weishan
AU - August, Avery
N1 - Publisher Copyright:
Copyright © 2015 by The American Association of Immunologists, Inc.
PY - 2015/3/15
Y1 - 2015/3/15
N2 - 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.
AB - 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.
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U2 - 10.4049/jimmunol.1402096
DO - 10.4049/jimmunol.1402096
M3 - Article
C2 - 25681342
AN - SCOPUS:84924567190
SN - 0022-1767
VL - 194
SP - 2477
EP - 2481
JO - Journal of Immunology
JF - Journal of Immunology
IS - 6
ER -