Sensing of cell-associated HTLV by plasmacytoid dendritic cells is regulated by dense β-galactoside glycosylation
Fig 5
Levels of pDC IFN-I production triggered by HTLV infected cells inversely correlate to the efficiency of infectious viral transmission via cell-cell contact.
A. IFN-I activity levels were quantified after co-culture of increasing number (2x103; 2x104; 2x105) of HTLV-1 (C91-PL; Hut102; MT-2) or HTLV-2 infected cells (C19; MO) with pDCs (2x104). The infected cells:pDC ratio is indicated on the right of the graph. Arrows indicate the maximum level of IFN-I activity for each cell line setting (mean of 3 independent experiments). B-G. Parallel representation of the maximum levels of IFN-I activity induced after co-culture of pDCs with HTLV-infected cells and of (B) intracellular viral RNA present in the cytoplasm of HTLV-infected cell lines (mean ± SD; 3 independent experiments); (C) viral RNA released in the supernatant of HTLV-infected cell lines after 24h of culture (mean ± SD; 3 independent experiments); (D) the percentage of cell contacts established between pDCs and HTLV-infected cells (mean ± SD; 2–4 independent experiments); (E) percentage of viral capture after 4h of co-culture with HTLV-1/2 infected cells as determined by p19gag detection in pDCs (mean ± SD; 3 independent experiments); (F) percentage of TRAIL expression after 24h of co-culture detected on the pDCs surface (mean ± SD; 3 independent experiments) or (G) maximum infectivity levels as determined in S5D Fig (n = 3). H. Correlation curve of pDC-dependent IFN-I production and viral transmission and calculated p value.