Journal
EUROPEAN RESPIRATORY JOURNAL
Volume 39, Issue 3, Pages 712-720Publisher
EUROPEAN RESPIRATORY SOC JOURNALS LTD
DOI: 10.1183/09031936.00099811
Keywords
Epithelial cell; immune response; respiratory viruses
Categories
Funding
- Wellcome Trust (London, UK) [063717, 083567/Z/07/Z]
- Wellcome Trust [063967]
- European Respiratory Society
- Asthma UK [02/027, 05/067]
- British Lung Foundation [P04/13, P06/3]
- British Lung Foundation/Severin Wunderman Family Foundation [00/02]
- Medical Research Council (London
- MRC) [G0601236]
- British Medical Association (HC)
- National Institute of Health Research Biomedical Research Centre (London)
- European Academy of Allergy and Clinical Immunology (EAACI
- Zurich, Switzerland
- Imperial College London
- Union Chimique Belge (UCB) Institute of Allergy (Brussels, Belgium)
- Asthma UK [05/067] Funding Source: researchfish
- Medical Research Council [G0601236, G1000758B, G1000758] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0508-10212, CL-2008-21-014] Funding Source: researchfish
- MRC [G0601236] Funding Source: UKRI
- Wellcome Trust [083567/Z/07/Z] Funding Source: Wellcome Trust
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The cytokine interleukin (IL)-15, major histocompatibility complex (MHC) class I molecules and MHC class I chain-related proteins (MIC) A and B are involved in cellular immune responses to virus infections but their role in respiratory syncytial virus (RSV) infection has not been studied. We aimed to determine how RSV infection modulates IL-15 production, MHC class I and MICA expression in respiratory epithelial cells, the molecular pathways implicated in virus-induced IL-15 production and how interferon (IFN)-gamma alters RSV-induced IL-15 production and MHC class I and MICA expression. We infected respiratory epithelial cell lines (A549 and BEAS-2B cells) and primary bronchial epithelial cells with RSV and measured production of IL-15, expression of MHC I and MICA and the role of the transcription factor nuclear factor (NF)-kappa B. We report here that RSV increases IL-15 in respiratory epithelial cells via virus replication and NF-kappa B-dependent mechanisms. Furthermore, RSV infection of epithelial cells upregulated cell surface expression of MICA and levels of soluble MICA. IFN-gamma upregulated RSV induction of soluble IL-15 but inhibited induction of MICA. Upregulation of IL-15, MHC I and MICA are likely to be important mechanisms in activating immune responses to RSV by epithelial cells.
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