Vaccine-induced protection against 3 systemic mycoses endemic to North America requires Th17 cells in mice

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.

Results

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.

Discussion

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.

Footnotes

See the related article beginning on page 554.