Correction to: Measles virus hemagglutinin triggers intracellular signaling in CD150-expressing dendritic cells and inhibits immune response

Correction to: Cellular & Molecular Immunology, https://doi.org/10.1038/cmi.2015.55, published online 15 June 2015

In this article, published online on 15 June 2015, there was an unintended error during the image processing of Figs. 2 and 4. In Fig. 2c, the time point 12 h was omitted and is included in the corrected Fig. 2c. Figure 4a and b contain blots not intended for that experiment, which now have been replaced with the blots generated for that experiment.

Fig. 2

CD150 modulates the Akt-signaling pathway in human DCs. DCs were cocultured with CHO/CHO-H cells a, c, d at a 1:5 ratio or stimulated with 10 μg/ml of anti-CD150 mAbs (clone IPO3) b at different times. Activation of signaling pathways via TLR2 and DC-SIGN receptors was blocked with specific anti-TLR2 c and anti-DC-SIGN d mAbs. FSL-1 was used as a specific ligand for TLR2 stimulation. Cell lysates were analyzed for pAkt (S473) expression by western blot with CD45 as a loading control. The level of pAkt was normalized against the level of CD45 using the TotalLab program e, f. e The results are expressed as the mean (±SD) from 3 to 6 independent experiments, and differences observed at 6, 12, and 24 h were statistically significant (*P < 0.05; **P < 0.001).

Fig. 4

CD150-mediated p38MAPK phosphorylation is decreased upon MV-H-CD150 interaction in DCs. DCs were either cocultured with CHO/CHO-H cells at a 1:5 ratio a, b or stimulated with 10 μg/ml of anti-CD150 IPO-3 antibody at different time points c. Activation of signaling pathways via the TLR2 receptor was blocked with specific anti-TLR2 antibodies d. Cell lysates were analyzed for pp38 MAPK (T180/Y182) expression by western blot with CD45 as a loading control. The level of ppMAPK38 was normalized against the level of CD45 using the TotalLab program e, f. e The results are expressed as the mean (±SD) from at least three independent experiments, and differences observed at 6 h were statistically significant (*P < 0.05, Student’s t test). g MP-1 cells were either stimulated with 10 μg/ml of anti-CD150 IPO-3 antibody or cocultured with CHO/CHO-H cells at a 1:5 ratio at different time points.

The conclusions drawn from the presented experiments remain unaltered, and this correction has no bearing on the final outcome of the study. The inconvenience caused by this error is deeply regretted.