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A Th17-polarized cell population that has infiltrated the lung requires cells that convert to IFN- production in order to induce airway hyperresponsiveness

A Th17-polarized cell population that has infiltrated the lung requires cells that convert to... Adoptive cell transfer of an ovalbumin (OVA)-specific Th17-polarized cell population from transgenic DO11.10 mice into BALB/c mice followed by OVA inhalation caused airway hyperresponsiveness (AHR) with severe neutrophilia. The transferred Th17 cell populationpreviously polarized in vitro with IL-6, transforming growth factor- and IL-23contained negligible numbers of IFN--producing cells; however, during Th17-cell-dependent airway inflammation, significant numbers of IFN--producing cellsincluding cells producing both IL-17 and IFN- and cells producing only IFN-were detected in the lung in addition to cells producing only IL-17. Using Th17-polarized cell populations derived from IL-17/ or IFN-/ mice, it was demonstrated that IL-17 is essential for inducing neutrophilic airway inflammation and that IFN- is required for the AHR elevation. IFN- appeared to be derived from cells producing both IL-17 and IFN- and/or from cells producing only IFN-, which were converted from the transferred Th17-polarized cell population. We also found that mAbs that neutralize IL-12 significantly suppressed the conversion of the Th17-polarized cell population toward IFN- producers in the lung; concomitantly, with this decreased conversion, IL-12 neutralization also attenuated the AHR elevation in the lung. IL-12-dependent conversion of the transferred Th17-polarized cell population into IFN- producers in the lung thus appeared to be a crucial process for inducing AHR elevation in Th17-cell-dependent airway inflammation. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png International Immunology Oxford University Press

A Th17-polarized cell population that has infiltrated the lung requires cells that convert to IFN- production in order to induce airway hyperresponsiveness

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References (56)

Publisher
Oxford University Press
Copyright
The Japanese Society for Immunology. 2010. All rights reserved. For permissions, please e-mail: [email protected]
ISSN
0953-8178
eISSN
1460-2377
DOI
10.1093/intimm/dxq034
pmid
20501609
Publisher site
See Article on Publisher Site

Abstract

Adoptive cell transfer of an ovalbumin (OVA)-specific Th17-polarized cell population from transgenic DO11.10 mice into BALB/c mice followed by OVA inhalation caused airway hyperresponsiveness (AHR) with severe neutrophilia. The transferred Th17 cell populationpreviously polarized in vitro with IL-6, transforming growth factor- and IL-23contained negligible numbers of IFN--producing cells; however, during Th17-cell-dependent airway inflammation, significant numbers of IFN--producing cellsincluding cells producing both IL-17 and IFN- and cells producing only IFN-were detected in the lung in addition to cells producing only IL-17. Using Th17-polarized cell populations derived from IL-17/ or IFN-/ mice, it was demonstrated that IL-17 is essential for inducing neutrophilic airway inflammation and that IFN- is required for the AHR elevation. IFN- appeared to be derived from cells producing both IL-17 and IFN- and/or from cells producing only IFN-, which were converted from the transferred Th17-polarized cell population. We also found that mAbs that neutralize IL-12 significantly suppressed the conversion of the Th17-polarized cell population toward IFN- producers in the lung; concomitantly, with this decreased conversion, IL-12 neutralization also attenuated the AHR elevation in the lung. IL-12-dependent conversion of the transferred Th17-polarized cell population into IFN- producers in the lung thus appeared to be a crucial process for inducing AHR elevation in Th17-cell-dependent airway inflammation.

Journal

International Immunology – Oxford University Press

Published: Jun 25, 2010

Keywords: airway inflammation IFN-γ IL-17 neutrophilia severe asthma

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