First published February 1, 2016 - More info
Marcel Wüthrich, Benjamin Gern, Chiung Yu Hung, Karen Ersland, Nicole Rocco, John Pick-Jacobs, Kevin Galles, Hanna Filutowicz, Thomas Warner, Michael Evans, Garry Cole, Bruce Klein
Original citation: J Clin Invest. 2011;121(2):554–568. doi:10.1172/JCI43984.
Citation for this corrigendum: J Clin Invest. 2016;126(2):795. doi:10.1172/JCI85788.
The authors recently became aware that the IL-1R mice used for the original Supplemental Figure 7, A and B, were incorrectly genotyped and were heterozygous rather than homozygous knockout animals. The experiment with IL1r–/– animals was repeated, and the correct Supplemental Figure 7 is now available online. The correct text describing the experiments in the Results and Discussion sections appears below.
Lung CFUs also were reduced to the same extent in vaccinated Il18r–/– and wild-type mice (Supplemental Figure 7B). In contrast, IL-17–producing T cells recruited to the lungs of IL1r–/– mice were reduced, and the mice failed to acquire resistance in comparison with vaccinated wild-type controls. Thus, IL-18R, but not IL-1R, is dispensable in the development of T17 cells and vaccine resistance. Moreover, failed T17 differentiation of 1807 cells in Myd88–/– mice is not due to impaired IL-18R signaling, but is likely due to impaired signaling via TLRs and IL-1R.
The fact that adoptively transferred wild-type 1807 cells failed to recruit to the lung in Myd88–/– mice and showed a deficit in IL1r–/–, but not Il18r–/–, mice indicates that the deficits in Myd88–/– mice are not due to impaired IL-18R signaling, but are likely due to impaired signaling via TLRs and IL-1R.
The authors regret the error.