Localization of Type I Interferon Receptor Limits Interferon-Induced TLR3 in Epithelial Cells
| Autor: | Ilona Jaspers, Luisa E. Brighton, Jonathan Ciencewicki |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Immunology
Stimulation Receptor Interferon alpha-beta Biology Downregulation and upregulation Interferon Cell Line Tumor Virology medicine Humans Receptor Regulation of gene expression virus diseases Epithelial Cells Research Reports Cell Biology Epithelium Toll-Like Receptor 3 Cell biology Solutions medicine.anatomical_structure Gene Expression Regulation Cell culture TLR3 Interferons medicine.drug |
| Zdroj: | Journal of Interferon & Cytokine Research. 29:289-297 |
| ISSN: | 1557-7465 1079-9907 |
| Popis: | Previous studies have shown that influenza infections increase Toll-like receptor 3 (TLR3) expression and that type I interferons (IFNs) may play a role in this response. This study aimed to expand on the role of type I IFNs in the influenza-induced upregulation of TLR3 and determine whether and how the localization of the IFN-alpha/beta receptor (IFNAR) in respiratory epithelial cells could modify IFN-induced responses. Using differentiated primary human airway epithelial cells this study demonstrates that soluble mediators secreted in response to influenza infection upregulate TLR3 expression in naive cells. This response was associated with an upregulation of type I IFNs and stimulation with type I, but not type II, IFNs enhanced TLR3 expression. Interestingly, although influenza infection results in IFN-beta release both toward the apical and basolateral sides of the epithelium, TLR3 expression is only enhanced in cells stimulated with IFN-beta from the basolateral side. Immunohistochemical analysis demonstrates that IFNAR expression is limited to the basolateral side of differentiated human airway epithelial cells. However, non- or poorly differentiated epithelial cells express IFNAR more toward the apical side. These data demonstrate that restricted expression of the IFNAR in the differentiated airway epithelium presents a potential mechanism of regulating type I IFN-induced TLR3 expression. |
| Databáze: | OpenAIRE |
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