NDLI: TH17 cells mediate steroid-resistant airway inflammation and airway hyperresponsiveness in mice.

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Year: 2008 Volume: 181 Issue: 5

Year: 2008 Volume: 181 Issue: 4

Year: 2008 Volume: 181 Issue: 3

Year: 2008 Volume: 181 Issue: 2

TH17 cells mediate steroid-resistant airway inflammation and airway hyperresponsiveness in mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Peterson, Alanna Irvin, Charles G. Piganelli, Jon D. Ray, Anuradha McKinley, Laura Kapadia, Shernaaz Henry, Adam Logar, Alison Kolls, Jay K. Alcorn, John F. Dupont, Rachel B.
Description	Country affiliation: United States Author Affiliation: McKinley L ( Department of Pediatrics, Lung Immunology and Host Defense Laboratory, University of Pittsburgh, Pittsburgh, PA 15213, USA.)
Abstract	Steroid-resistant asthma comprises an important source of morbidity in patient populations. T(H)17 cells represent a distinct population of CD4(+) Th cells that mediate neutrophilic inflammation and are characterized by the production of IL-17, IL-22, and IL-6. To investigate the function of T(H)17 cells in the context of Ag-induced airway inflammation, we polarized naive CD4(+) T cells from DO11.10 OVA-specific TCR-transgenic mice to a T(H)2 or T(H)17 phenotype by culturing in conditioned medium. In addition, we also tested the steroid responsiveness of T(H)2 and T(H)17 cells. In vitro, T(H)17 cytokine responses were not sensitive to dexamethasone (DEX) treatment despite immunocytochemistry confirming glucocorticoid receptor translocation to the nucleus following treatment. Transfer of T(H)2 cells to mice challenged with OVA protein resulted in lymphocyte and eosinophil emigration into the lung that was markedly reduced by DEX treatment, whereas T(H)17 transfer resulted in increased CXC chemokine secretion and neutrophil influx that was not attenuated by DEX. Transfer of T(H)17 or T(H)2 cells was sufficient to induce airway hyperresponsiveness (AHR) to methacholine. Interestingly, AHR was not attenuated by DEX in the T(H)17 group. These data demonstrate that polarized Ag-specific T cells result in specific lung pathologies. Both T(H)2 and T(H)17 cells are able to induce AHR, whereas T(H)17 cell-mediated airway inflammation and AHR are steroid resistant, indicating a potential role for T(H)17 cells in steroid-resistant asthma.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	6
Volume Number	181
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2008-09-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Bronchial Hyperreactivity Immunology Pathology Dexamethasone Pharmacology Drug Resistance Interleukin-17 Metabolism Receptors, Interleukin-17 Physiology T-lymphocyte Subsets Th2 Cells Animals Prevention & Control Cells, Cultured Chemokines Secretion Chemotaxis, Leukocyte Clone Cells Disease Models, Animal Lung Mice Mice, Inbred Balb C Mice, Knockout Mice, Scid Mice, Transgenic Deficiency Genetics Transplantation Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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