Expression data from human iNKT cells with or without interaction with human airway epithelium

Recent studies showing involvement of iNKT cells in lung viral infections and airway inflammation suggest that these cells are key players in both prevention and generation of immune-pathology in the lungs. It is not fully understood how iNKT cells are activated in the lungs and if this relied solely on lung dendritic cells. We recently showed that CD1d is expressed on airway epithelium, and now demonstrate that iNKT cells can be activated by primary airway epithelial cells, via both CD1d dependent and independent processes. Transcriptional analysis of human iNKT cells reveals that direct contact with lipid-pulsed primary human airway epithelial cells results in initiation of a programme of activation comprising rapid and concomitant induction of cytokine genes and genes to switch off this response. These findings establish a new mode of activation within the lungs for iNKT cells, and further enhance the role of airway epithelium in innate lung immunity. Human iNKT cells (an in vitro expanded clone [LH22]; Ho et al, 2004) were selected at three conditions for RNA extraction and hybridization on Affymetrix Gene ST 1.0 microarrays. For baseline, we used iNKT cells which had not been exposed to airway epithelium ('untouched' - iNKT_0h). Then, we studied the biological processes that occur in iNKT cells after interaction with human airway epithelium. For this, we pulsed normal human bronchial epithelial (NHBE) cells with αGC for 24 hours, then co-cultured these with iNKT cells directly (‘Direct’ - iNKT_Direct_4h) or separated by Transwell™ inserts (‘Transwell’ - iNKT_Transwell_4h). Three biological replicates were studied at each condition.