4.6 Article

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

Journal

JOURNAL OF IMMUNOLOGY
Volume 182, Issue 8, Pages 4507-4511

Publisher

AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0900237

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Funding

  1. NCRR NIH HHS [P20RR017670, P20 RR017670, P20 RR017670-03] Funding Source: Medline
  2. NHLBI NIH HHS [R01 HL079189, R01 HL079189-03, R01-HL079189, R01 HL079189-04] Funding Source: Medline
  3. NIGMS NIH HHS [P30 GM103338] Funding Source: Medline

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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 Journal of Immunology, 2009,182:4507-4511.

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