HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Data Supplement Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Jaffar, Z. Articles by Roberts, K. Search for Related Content PubMed PubMed Citation Articles by Jaffar, Z. Articles by Roberts, K.

Cutting Edge: Lung Mucosal Th17-Mediated Responses Induce Polymeric Ig Receptor Expression by the Airway Epithelium and Elevate Secretory IgA Levels ¹

Center for Environmental Health Sciences, Biomedical and Pharmaceutical Sciences, University of Montana, Missoula, MT 59812

Polymeric Ig receptor (pIgR) is a central player in mucosal immunity that mediates the delivery of polymeric IgA and IgM to the apical surface of epithelial cells via transcytosis. Emerging evidence suggests that Th17 cells not only mediate autoimmunity but also play key roles in mucosal host defense against pathogens. We demonstrate that OVA-specific CD4⁺ Th17 cells, in addition to causing neutrophilic inflammation in mice, mediated a pronounced influx of CD19⁺ B cells into the lungs following Ag inhalation. Coincident with this recruitment was a striking induction in pIgR expression by the bronchial epithelium and a subsequent increase in airway IgM and secretory IgA levels. Intranasal administration of IL-17 revealed a crucial role for this cytokine in inducing pIgR expression by the epithelium. These findings support a key role for Th17 cells in pulmonary immune defense against respiratory pathogens by promoting pIgR-mediated transport of secretory IgA and IgM into the airway.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grant R01-HL079189 and Center of Biomedical Research Excellence (COBRE) Grant P20RR017670.

² Z.J. and M.E.F. contributed equally to this article.

³ Address correspondence and reprint requests to Dr. Kevan Roberts, Center for Environmental Health Sciences, 285B Skaggs Building, University of Montana, Missoula, MT 59812. E-mail address: kevan.roberts{at}umontana.edu

⁴ Abbreviations used in this paper: SIgA, secretory IgA; BAL, bronchoalveolar lavage; LMC, lung mononuclear cell; pIgR, polymeric Ig receptor; SC, secretory component.

⁵ The online version of this article contains supplemental material.